I have kept an informal ledger of my own desire for decades. Not a diary exactly. More the kind of running tally you keep of anything you find fascinating. And the thing the ledger taught me long before any study did is that desire does not behave like a hormone chart. It surges and slumps for reasons that have nothing to do with the number on a blood test. Stress flattens it. A good week lifts it. Certain plants, in my experience, send lust through the roof.
Then in January 2026 a team at the University of Tartu in Estonia published the largest study of sexual desire ever run1 and it said, in numbers, what my ledger had been saying in scribbles. Men’s desire does not fade from the twenties as the testosterone story predicts. It peaks around 40. And the gap between the hormone story and the real one is where everything interesting about desire lives.
So this post is in two halves. The first is what the study found. The second is the question it leaves hanging: if testosterone isn’t your sex drive, what is? That question happens to be the whole reason this blog exists.
What 67,000 people said
The Estonian Biobank holds around a fifth of the country’s adult population. Between November 2021 and April 2022, 67,334 members aged 20 to 84 answered two plain questions: how strongly they agreed that “I have strong sexual urges” and that “I do not think much about sex”.1 The two answers were combined into a single desire score. Seven in ten respondents were women. Three quarters lived with a partner. It is a study of everybody. Not of people with a problem.
Men’s desire rose through the twenties and thirties, peaked in the late thirties and early forties and only fell back to twenty-something levels after 60.1 The researchers called this “surprising” and admitted it contradicted their own prediction of a straight decline. Their explanation, and they offer it as a possibility rather than a finding, is life rather than biology: men in their forties are more likely to be in stable relationships, and in this data living with a partner went with higher desire in men. The study cannot tell whether a partner raises lust or whether lustier men are more likely to be partnered. It is an assertion, and I would hold it loosely.
Men also reported more desire than women at every age, and the gap widened with each decade, from 0.59 in the study’s units among the under-30s to 1.14 at 60 and over.1 Women’s desire peaked in their twenties and fell more steeply, especially after 50. The authors are careful to say these are averages and that at any age plenty of women want sex more than most men. But if you are half of a long relationship and your appetites no longer match, that is the statistical norm. Not a fault in either of you.
Two honest limits. The measure is two questions and self-reported, and the study compares different people at different ages rather than following the same people for decades, so some of the curve could be generational. Even so, nothing on this scale has been done before.
Testosterone sets a floor. That is all it does.
Here is the part that matters. Everything the researchers knew about a person (age, gender, orientation, relationship, children, education, job) explained 28% of the differences in desire.1 Testosterone was not measured, but three other studies tell you what would have happened if it had been.
A 2012 study of 196 healthy adults looked for a link between testosterone and desire in men and found none.2 What did explain the gap between men and women was how often people masturbated. Behaviour, not blood. A 2024 study went further: 41 young men gave a saliva sample every day for a month and rated their desire each day.3 A man’s testosterone on a given day told you nothing about how much he wanted sex that day. What it did track was courtship effort on days single men met someone they fancied. Testosterone, it seems, is for pursuit rather than appetite.
The hormone is not irrelevant. A 2026 study of 526 older European men found that measured free testosterone (the small unbound fraction, not the total on most blood tests) did track desire, orgasm frequency and erections, but only below a threshold of roughly 140 to 160 pmol/L.4 Below that floor lust suffers and treatment helps. Above it the number tells you very little.
I can vouch for the floor. I have been on testosterone replacement for years. It helps with libido and energy and it fights the brain fog. I would not stop it. But I am still overweight and it has not turned me into a muscle-bound love machine. It fixed the floor. It did not build the house. And the difference between the two is the difference between hormone medicine and the chemistry of wanting.
If testosterone isn’t your sex drive, what is?
Desire is run by the brain, and the brain runs it on a handful of chemicals that most sex-drive articles never mention. A 2009 review by the sex researcher James Pfaus drew the map.5 The accelerator is dopamine, the wanting chemical, helped by oxytocin and noradrenaline. The brake is serotonin, along with the brain’s own opioids. Lust is what you get when the accelerator is pressed and the brake is off. Testosterone’s job is to keep the accelerator wired up. It does not press it.
Once you see it this way, the things that move lust in real life stop being mysterious.
Stress presses the brake. A 2025 study from Vienna had 63 men and women in relationships rate stress and desire six times a day for two weeks and spit into a tube each time for cortisol.6 Higher stress went with lower desire and arousal in the moment, and higher cortisol went with lower desire more strongly in women than in men. Which is worth knowing if your partner’s desire vanishes in a hard month and yours doesn’t.
Sleep, or the lack of it, presses the brake too, and by a route I found startling. A 2026 study kept male rats short of sleep and found it shifted the brain’s use of tryptophan away from making serotonin and toward a pathway linked to irritation in the body instead. The rats reached climax faster, a sign of disturbed control, and blocking that pathway reversed it.7 In men, a 2026 review of nine studies found those with sleep apnoea had testosterone around a third of the level seen in shift workers with disturbed sleep, and even mild apnoea dented erections.8 Poor sleep hits both the floor and the brake at once.
Then there is serotonin itself. Antidepressants that raise serotonin are the clearest human evidence that the brake is real: a 2009 analysis of the trials found sexual side effects in anywhere from 26% to 80% of patients depending on the drug, with desire, arousal and orgasm all affected.9 Nobody on those drugs has less testosterone. They have more brake.
And the strangest evidence of all runs the other way. MDMA, the illegal drug better known as ecstasy, floods the brain with serotonin and oxytocin at once. A 2023 systematic review of fourteen studies found it generally increased lust in both sexes and made orgasm more intense when it arrived, while delaying it and sometimes impairing erections in men.10 Anyone who was around in the early nineties will not need fourteen studies to tell them that. I am not recommending it. It is illegal almost everywhere and hard on the brain. But it is the most vivid demonstration there is that a shift in brain chemistry can produce more lust than any hormone ever has.
And the map is not finished. Pfaus’s review already lists players most people have never heard of: noradrenaline, the brain’s own opioids, its own cannabis-like chemicals, and a family of signals called melanocortins that a licensed desire drug for women works on. The newest name is kisspeptin, a brain hormone only discovered this century. In a 2023 placebo-controlled trial at Imperial College London, 32 men with low sexual desire were given it by infusion while they watched erotic film. It changed activity across the brain’s sexual-processing network, increased erections by up to 56% over placebo and lifted the men’s reported desire.14 The authors called it the first candidate drug for low desire in men. Nobody yet knows which plants, if any, act on it, or on the gut bacteria that a handful of 2026 studies are starting to link to sexual function. Which is to say the list of things that move lust is still being written, and testosterone is one line on it.
My own ledger has an entry that belongs here. Some years ago I had a course of traditional Chinese medicine, acupuncture and herbs together, for reasons unconnected with sex. The effect on my lust was monumental. I still do not know which part did it and the published evidence for acupuncture and desire is thin, so take this as one man’s honest report rather than a finding. But it is the kind of report that keeps me curious.
Why I keep coming back to plants
If desire lives in the accelerator and the brake rather than in testosterone, then the interesting question about any herbal aphrodisiac is not “does it raise testosterone?” It is “which pedal does it touch?”
Fenugreek, which I wrote about last time, does nudge free testosterone, and the best trial found that this made no difference to desire at all.11 That was the first clue. Maca is the opposite case: a 2002 placebo-controlled trial gave men 1.5 or 3 grams a day for 12 weeks and found their desire rose from week eight while their testosterone did not move at all.12 Something other than the hormone was doing the work. Ashwagandha is a brake-lifter: a 2019 trial in stressed adults found it cut morning cortisol against placebo,13 which is the stress chemical we met three paragraphs ago. Damiana and horny goat weed have thinner evidence and a longer folklore, and each will get its own honest post.
That is the project. Not chasing a hormone, but mapping which plants press the accelerator, which lift the brake, and what the trials say when you read them properly.
What this means in practice
The bottom line. If your testosterone is normal, stop chasing it. Adding more will not add desire. The Estonian study, the daily-saliva study and the 526 older men all say the same thing.
If you suspect it is low, and the signs are low desire together with low energy and fog rather than low desire alone, ask your doctor for a free testosterone measurement, not a total. Total predicted nothing in the 2026 study. Free did.4 If it is under the floor, treatment helps. I am the evidence.
Then work the pedals on lust itself. Sleep is first because it hits the floor and the brake together. Stress is second, and if you are on an antidepressant that flattens desire, that is a conversation to have with your doctor rather than something to accept. After that come the plants, and maca is the best-evidenced place to start for lust that has gone quiet without a hormone problem behind it. Three grams a day, eight weeks before you judge it.
As for the study that started all this: I was never the oddity my ledger suggested. I was the average. The interesting part was never the peak. It was what the peak proved about the hormone everyone blames.
Citations
1. Aavik T, Täht K, Vainik U, Mõttus R. Associations of Sexual Desire with Demographic and Relationship Variables. Sci Rep. 2026;16(1):215. https://pmc.ncbi.nlm.nih.gov/articles/PMC12769728/
2. van Anders SM. Testosterone and sexual desire in healthy women and men. Arch Sex Behav. 2012;41(6):1471–1484. https://pubmed.ncbi.nlm.nih.gov/22552705/
3. Catena T, Crewther BT, Eisenbruch AB, Grillot RL, Maestripieri D, Roney JR. Day-to-day associations between testosterone, sexual desire and courtship efforts in young men. Proc Biol Sci. 2024;291(2035):20241508. https://pmc.ncbi.nlm.nih.gov/articles/PMC11597408/
4. Narinx N, David K, Walravens J, et al. Low measured free testosterone is associated with worse sexual function in community-dwelling men. Eur J Endocrinol. 2026;195(2):293–301. https://pubmed.ncbi.nlm.nih.gov/42530279/
5. Pfaus JG. Pathways of sexual desire. J Sex Med. 2009;6(6):1506–1533. https://pubmed.ncbi.nlm.nih.gov/19453889/
6. Mües HM, Markert C, Feneberg AC, Nater UM. Too stressed for sex? Associations between stress and sex in daily life. Psychoneuroendocrinology. 2025;181:107583. https://pubmed.ncbi.nlm.nih.gov/40907147/
7. Cao Z, Zhu T, Ge Y, et al. Chronic Sleep Deprivation Accelerates Ejaculation by Shifting Brain Tryptophan Metabolism Toward the Kynurenine Pathway in Male Rats. Andrology. 2026. https://pubmed.ncbi.nlm.nih.gov/42578609/
8. Almurayyi M, Alshahrani ST, Alshardi WI, et al. Sleep disorders and male sexual dysfunction: a meta-analysis of hormonal and erectile outcomes. Arch Ital Urol Androl. 2026;15659. https://pubmed.ncbi.nlm.nih.gov/42707009/
9. Serretti A, Chiesa A. Treatment-emergent sexual dysfunction related to antidepressants: a meta-analysis. J Clin Psychopharmacol. 2009;29(3):259–266. https://pubmed.ncbi.nlm.nih.gov/19440080/
10. Wexler A, Dubinskaya A, Suyama J, Komisaruk BR, Anger J, Eilber K. Does MDMA have treatment potential in sexual dysfunction? A systematic review of outcomes across the female and male sexual response cycles. Sex Med Rev. 2023;12(1):26–34. https://pubmed.ncbi.nlm.nih.gov/37888490/
11. Lee-Ødegård S, Gundersen TE, Drevon CA. Effect of a plant extract of fenugreek on testosterone in blood plasma and saliva in a double blind randomized controlled intervention study. PLoS One. 2024;19(9):e0310170. https://pmc.ncbi.nlm.nih.gov/articles/PMC11407615/
12. Gonzales GF, Córdova A, Vega K, et al. Effect of Lepidium meyenii (MACA) on sexual desire and its absent relationship with serum testosterone levels in adult healthy men. Andrologia. 2002;34(6):367–372. https://pubmed.ncbi.nlm.nih.gov/12472620/
13. Lopresti AL, Smith SJ, Malvi H, Kodgule R. An investigation into the stress-relieving and pharmacological actions of an ashwagandha (Withania somnifera) extract: A randomized, double-blind, placebo-controlled study. Medicine. 2019;98(37):e17186. https://pmc.ncbi.nlm.nih.gov/articles/PMC6750292/
14. Mills EG, Ertl N, Wall MB, et al. Effects of Kisspeptin on Sexual Brain Processing and Penile Tumescence in Men With Hypoactive Sexual Desire Disorder: A Randomized Clinical Trial. JAMA Netw Open. 2023;6(2):e2254313. https://pmc.ncbi.nlm.nih.gov/articles/PMC9898824/
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