What Bryan Johnson Accidentally Got Right

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19 Min Read


Sara Szal MD

A few weeks ago, Bryan Johnson, the tech billionaire reportedly spending two million dollars a year trying not to die, posted his girlfriend Kate Tolo’s vaginal microbiome score to his million-plus followers minutes after announcing he had just performed oral sex on her.

He called the post an exercise in transparency. The internet called it something else. I thought to myself, “This is an important cultural moment, does Kate give informed consent, and also ick.”

Within 48 hours a phrase had entered the cultural vocabulary: coochie carfax.

A coochie carfax is what it sounds like: the full report card for a woman’s vaginal ecosystem, what lives there, what is protecting her, and what is missing. The internet meant it as a joke.

The biology it describes is not a joke, it is 30 years of research that medicine never bothered to explain to the women it most affects.

Let me sit with that phrase before I say anything clinical, because it is doing something that decades years of women’s health advocacy, public health campaigns, and gynecology education have collectively failed to do… it is making people care.

We can criticize the larger issues around the cultural moment. What Johnson practiced was disclosure of a woman’s intimate biology as a feature of his own optimization story. Her body was the data point. His protocol is still the headline. A man posting his partner’s vaginal microbiome score immediately after announcing he performed oral sex on her collapses the distance between intimacy and content. It treats a woman’s body as both a sexual object and a health metric in the same breath, and publishes both simultaneously to optimize engagement. The framing positions female biology as something to be tracked, scored, and reported by the person adjacent to it rather than the person living inside it, which is not a new dynamic. Medicine has practiced a version of it for decades: the woman’s body as a site of male interpretation rather than female self-knowledge. Johnson updated the interface but the power structure is the same.

It is a power structure I am on a mission to upend.

Yet the coochie carfax moment is making people ask what the report shows, what the scores mean, and why some women have what Kate has and most do not.

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I do not care about Bryan Johnson and his wellness diary. What I care about is the 70 percent of reproductive-age women who do not have what his girlfriend has, who have never had a coochie carfax, who have never been told that L. crispatus exists or that its absence is an important clinical fact with broad clinical consequences. [1]

I care about the women who sat in my exam room year after year with recurrent bacterial vaginosis, recurrent yeast, the unspecified burning that showed nothing that I could detect under the microscope. More often than not, those women received another course of the same drug that had not worked the last time. They were not offered them a report card or an assessment of their ecology. Nobody offered them the framework that would have explained why the treatment kept failing.

That is the story, not the billionaire and his girlfriend’s score. The 70 percent.

Lactobacillus crispatus is the organism that, when dominant, works as the archetypal bouncer and immune modulator of the vaginal compartment. It produces lactic acid and hydrogen peroxide, holds vaginal pH below 4.5, and actively suppresses the low-grade inflammation that bacterial vaginosis and dysbiosis generate. When it owns the space, almost nothing pathogenic can replicate there. When something displaces it and diversity enters, what follows is exactly what half my patient panel had: burning, odor, recurrence, and the grinding circular treatment protocol that never addressed the real problem.

Mainstream medicine did not give those women a coochie carfax, it gave them metronidazole or fluconazole. Again.

The spectacle was easy to mock. A billionaire optimizing his girlfriend’s cervicovaginal ecology and posting the results is, at minimum, a lot. And yet the science he stumbled into is real. Kate Tolo scored a 100 because her vaginal microbiome is 98.7 percent L. crispatus. Bryan Johnson concluded that this sits downstream of everything: sleep, glucose, stress, gut health, what you eat, what you put inside you. He is right, he just announced it in the most Bryan Johnson way imaginable.

Here is the part that went unnoticed in the pile-on. The oral sex Bryan Johnson performed on Kate, and broadcast in the same breath as her score, is one of the most consistently documented disruptors of the very ecosystem he was celebrating. I come back to that below, with the studies, because the timing was almost too perfect and the mechanism is real.

The question this essay is built to answer is not whether Bryan Johnson’s social media habits are appropriate, which they are not. The question is what it means that 70 percent of reproductive-age women don’t have what his girlfriend has, and what medicine has failed to tell them about why they don’t have it already. [1] What happened to their L. crispatus? Where did it go, and who failed to tell them it was gone?

The comments that came into my practice and to this newsletter after I published the first two pieces on vaginal microbiome science answered that question in ways no journal article can. They came from nurses, from microbiologists, from 71-year-old women with recurrent UTIs who had been told to stop having sex and wear Depends. From a woman who almost flew to Spain for a UTI vaccine because American urology had nothing left to offer her. From a physician who has practiced for thirty years and still heard herself say there was so much I did not know how to offer.

This essay is a continuation of that conversation. It is about what the viral moment revealed, what the readers revealed, and what the research says about the women who have the least and need the most, women in and after menopause.

The phrase caught because it named something that had no name. A woman’s complete vaginal microbiome profile, the ecological record of what lives there, what defends it, and what has displaced the defense, is not a concept that exists in ordinary medical conversation. Your gynecologist has never offered you a coochie carfax. Most gynecologists have never ordered a vaginal microbiome sequencing test, because most insurance panels don’t cover it, most training programs don’t teach it, and most clinical guidelines still organize vaginal health around pathogens rather than ecological community state.

Kate Tolo’s score is remarkable, but not because it is exceptional biology. It is the biology every woman’s vaginal ecosystem is built to achieve, and most never reach it. Not because their bodies failed, but because the terrain was never supported, the disruptions were never named, and the tools to rebuild were never offered. Only about 25 to 30 percent of reproductive-age women hold the L. crispatus-dominant community state, CST I, that Tolo’s score reflects. [1] The rest live in varying states of ecological instability that medicine has either overtreated with antibiotics, undertreated with a shrug, or never tested for at all.

A reader who works as a microbiologist: I understood the L. crispatus influence on the vaginal environment, but I had never made the connection to what was happening to my own body in perimenopause. The science was in my head and the symptoms were in my body and I had no bridge between them.”

That gap, between what the science knows and what women have been told, is the indictment. Not of individual clinicians, many of whom work inside systems that never gave them the vocabulary, the time, or the tools, but of a model of women’s health that organized thirty years of vaginal medicine around swab cultures and antimicrobial prescriptions without once asking why the protective community keeps collapsing and what it would take to rebuild it.

The coochie carfax went viral because it answered a question women had been asking their doctors for years without getting an answer. Not what infection do I have, but why do the infections keep coming, and when does my body get back to what it was before.

For many women, the body has never had a clear path back. Until the 2025 randomized controlled trial my colleagues and I published, it was not clear one existed. That trial showed a multi-strain L. crispatus vaginal synbiotic converted 90 percent of women with dysbiosis to CST I dominance, against 11 percent of placebo recipients. [2] That result is proof, not a nudge: the defended state is recoverable, and the body, given the organism it needs, will rebuild the ecology it was designed to maintain.

But recovering the defended state at 35 is a different clinical problem from recovering it at 58. That is the conversation I want to have.

The culture came back negative. The microscope showed nothing. She has been trying to tell us something for years. Medicine built the wrong instrument to hear it.

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In the middle of the spectacle, Kate Tolo made a point that deserved more clinical airtime than it got. She used the thread to say that oral sex is a real vaginal microbiome disruptor. Saliva changes vaginal pH and shifts microbial composition, and the oral cavity is a vector for sexually transmitted infections that rarely comes up in a gynecology visit. She was right, and the evidence behind her is stronger and older than most clinicians realize.

Here is the irony the pile-on missed. The oral sex Bryan Johnson performed on Kate, and posted about in the same breath as her score, is one of the most consistently identified independent risk factors for bacterial vaginosis in the literature. He was optimizing and disrupting the same ecosystem on the same night.

The prospective data is not ambiguous. In a 1999 cohort that followed 51 women with daily diaries and self-collected vaginal smears, receptive oral sex was the only behavior that stayed significantly associated with unstable vaginal flora in multivariate analysis, ahead of number of partners, condom use, and frequency of vaginal intercourse. [3] In a 24-month cohort of 298 women who have sex with women, receptive oral sex carried an adjusted hazard ratio of 3.52 for incident BV, a stronger association than acquiring a new sexual partner and second only to having a partner with BV symptoms. [4] A separate cohort in the same population found a dose-response relationship, where each additional episode of receptive oral-vulvovaginal sex raised the hazard of BV acquisition. [5] A longitudinal study of 617 women identified cunnilingus at the last sexual encounter as one of the behaviors associated with altered vaginal microflora. [6]

The mechanism is not a mystery, and it has a molecular basis. Fusobacterium nucleatum, one of the most abundant bacteria in the human mouth, shows up frequently in the vaginal microbiome of women with BV and is rare in healthy vaginal flora. F. nucleatum cannot harvest the sialic acid nutrients it needs on its own. In a BV-like environment, where sialidase-producing bacteria like Gardnerella vaginalis are present, it thrives through glycan cross-feeding, and then it supports the outgrowth of Gardnerella in return, building a mutually reinforcing dysbiotic loop. The researchers who mapped this were explicit that the ubiquity of F. nucleatum in the mouth points to a mechanism linking vaginal dysbiosis and oral sex. [7] A 16S sequencing case report documented both oral and vaginal sex altering a couple’s microbiota, with oral sex specifically increasing organisms that displace Lactobacillus. [8] The oral cavity is a reservoir of the same anaerobes that define BV, Prevotella, Fusobacterium, Porphyromonas, and Veillonella, and oral-genital contact is a direct route for moving them into the vaginal niche. [9]

This is why a growing body of work reframes BV not as a classic sexually transmitted infection but as a sexually enhanced disease, in which Gardnerella carriage is boosted by non-penetrative contact, including oral sex, rather than by a single transmitted pathogen. [9] A 2025 expert review concluded that sexual activity is the predominant mode of initial BV acquisition, and that non-coital behaviors, oral sex among them, are part of that picture. [10]

What I was taught in medical school: the vaginal ecosystem is sealed. What thirty years of practice have shown me: it is a negotiated ecology, shaped by everything that enters it, including the oral microbiome of every partner, a variable medicine has never thought to name.

Now the indictment. The evidence I just walked through spans 25 years. The guidelines the average gynecologist practices from have not caught up. The ACOG practice bulletin on vaginitis recognizes that BV is associated with sexual activity broadly, but does not name receptive oral sex as an independent risk factor. [11] The CDC treatment guidelines do the same, listing sexual activity in general and stopping there. [12] So a woman with recurrent BV sits across from a clinician trained on documents that never mention the one behavior with the most consistent prospective signal, and she is handed another course of metronidazole without a single question about her sexual practices.

One reader: I figured out on my own that something about unprotected sex was destabilizing my vaginal environment. I brought it up with three different gynecologists over five years. None of them asked me anything about it.”

I believe every woman with recurrent BV deserves to be asked about oral sex, partner microbiome, and barrier use before she is handed one more prescription.

The vaginal ecosystem is a negotiated one. What enters it matters and who enters it matters. Medicine almost never has this conversation with women, and the reason is structural. The model treats the vagina as sealed off from everything that touches it.

★ Post continues for paid subscribers ★

That conversation has three parts, and each one is information your physician has almost certainly never offered you.

Behind the paywall: what happens to L. crispatus at menopause, stated in clinical terms rather than the language of dryness and aging. What the data shows about vaginal estradiol and DHEA, what each one does and what each one leaves unfinished. And the sequenced intervention strategy, substrate first, then organism, that has strong mechanistic support and no equivalent in current gynecology guidelines.

I also want to document what came into this newsletter after the first two pieces. The comments read less like a comment section and more like a clinical history: a woman who almost flew to Spain for a UTI vaccine that does not exist in this country, a 71-year-old told to stop having sex and wear Depends, a clinician of thirty years who wrote that there was so much I did not know how to offer. These are not edge cases. They are the pattern. And the pattern has a clinical explanation medicine has not yet delivered.

If you have cycled through the same treatments without ever being told what the ecology needs, what you are about to read is why.



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