This essay is a companion to “What Is ADHD? An Essay on the Making of a Childhood Disease” and to “The Arithmetic Pill.” The first essay traced the pediatric symptom cluster to environmental exposures the diagnostic apparatus refuses to investigate. This one follows the adult female wave of the same diagnosis to a specific drug the medical system has been prescribing to teenage girls for six decades. The frame is two drugs. The first drug is the pill, taken every day from adolescence into the thirties. The second drug is the stimulant prescribed for the executive dysfunction that follows. Establishment terminology (ADHD, neurodevelopmental disorder, adverse events, mood changes) appears in attribution, quotation, and the reference titles the essay depends on. The analytical voice operates in a different register, treating the executive dysfunction the diagnosis captures as a documented consequence of a documented exposure rather than as an inherent brain disorder discovered late in adult women.
The Conception Cliff
There is a pattern women describe when they come off long-term hormonal contraception before trying to conceive. Their thinking gets clearer over the following months. Their moods settle. They notice their skin, their appetite, their libido, their response to stress, their attraction to their partner. Something they had understood to be their baseline personality turns out to have been the drug.
The pattern is not confined to isolated reports. Reproductive endocrinologists observe it in the clinics that specialize in helping women conceive. Direct-to-consumer women’s health writers have built practices and readerships around documenting it. Sarah Hill, a research psychologist at Texas Christian University who spent years studying female hormonal cognition without noticing she was on the pill herself, writes in This Is Your Brain on Birth Control that she did not understand what the drug had done to her until more than a year after she stopped taking it.¹ Naturopath Jolene Brighten built a clinical practice around what she calls post-birth-control syndrome, the collection of symptoms that emerge in the months after discontinuation and the parallel collection that resolves.
The observation is testable in the reader’s own life. She has, most likely, at least one friend or family member who has come off the pill after long-term use, whether to conceive or simply to find out what the drug was doing. The friend will report the pattern. Reproductive clinics document it as routine.
What the observation isolates is the pill itself as the variable. Same woman, same job, same relationships, same diet, same city, same age. The only difference is the daily tablet of synthetic estrogen and synthetic progestin. When the tablet stops, the woman changes. What she changes back into is closer to what her body would have been all along, absent the drug she was given at fifteen for acne or dysmenorrhea or irregular cycles and continued out of habit and convenience for the fifteen years that followed.
If a woman’s baseline personality can shift meaningfully after discontinuation, the drug is doing something to her while she is on it.
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The First Drug
The pill overrides a woman’s hormones rather than fine-tuning them. The synthetic estrogen (ethinyl estradiol) and synthetic progestin (varying between formulations) that a woman on combined oral contraceptives takes each day suppress the hypothalamic-pituitary-ovarian axis. Her ovaries stop cycling. Her endogenous estrogen and progesterone production is switched off. Her body enters a chronic pharmacological state that would occur nowhere in nature: continuous levels of synthetic sex steroids that bind and suppress the receptors that would ordinarily respond to her own hormones.
The clinical effect is that she does not ovulate. The neurological effect is that her brain, which has estrogen and progesterone receptors distributed throughout every major system, is now receiving a signal that has nothing to do with her body’s own reproductive rhythm and everything to do with the pharmaceutical dose the tablet delivers.
The consequences for cognition follow from what estrogen and progesterone normally do in the brain. Estrogen modulates dopamine, the neurotransmitter that underlies motivation, focus, novelty-seeking, and the sense of reward. It does so through direct receptor action in the prefrontal cortex and striatum, and through modulation of dopamine synthesis, release, and reuptake. When endogenous estrogen is suppressed and replaced with a synthetic analog that binds different receptors with different affinities, the dopamine signaling that depends on the natural molecule is disrupted. What follows in the affected woman is a diffuse reduction in the drive, focus, and reward response that would ordinarily support sustained attention and task completion.
Progesterone’s metabolite allopregnanolone is a positive allosteric modulator of the GABA-A receptor, the brain’s primary inhibitory system. When endogenous progesterone is cycling, allopregnanolone modulates GABA in ways that support the natural rhythm of mood, sleep, and stress response. When endogenous progesterone is suppressed and replaced with a synthetic progestin that does not produce allopregnanolone, the GABA modulation that depended on it is lost. Hill and others have documented what follows: mood dysregulation, sleep disruption, anxiety, and the blunting of the cortisol stress response that normal cycling supports.²
The prefrontal cortex, where executive function is generated, is particularly vulnerable to this class of interference. Its development is not complete at fifteen, when the typical first prescription is written, nor at twenty-five, when a woman may already have been on the drug for a decade. Prefrontal maturation, which includes myelination, synaptic pruning, and the establishment of the top-down control networks that will govern her adult attention and decision-making, continues into the late twenties. Continuous suppression of the sex hormones that guide this maturation during exactly the years the maturation is happening is not a neutral intervention.
The research establishing this at the mechanism level is recent and continues to accumulate. Rachel Gilfarb and colleagues at Ohio State University published two 2025 papers using a validated rodent model of adolescent HC exposure. In the first, published in Brain, Behavior, and Immunity, they demonstrated that adolescent rats given daily ethinyl estradiol and levonorgestrel throughout their adolescent equivalent showed decreased microglia in the medial prefrontal cortex, altered microglia morphology, and reduced expression of genes related to phagocytosis and neuroimmune signaling in the same region.³ Microglia are the phagocytic cells of the developing brain, and their role in adolescent prefrontal maturation includes synaptic pruning and the shaping of mature cortical circuitry. In the second paper, published in Hormones and Behavior, the same team showed that the same exposure altered expression of genes related to synapses, white matter, monoamine signaling, and hormone signaling in the medial prefrontal cortex and hypothalamus, and that behaviorally the treated rats showed diminished risk assessment and altered anxiety-like behavior.⁴
The human parallel is documented in the Adolescent Brain Cognitive Development Study, an ongoing longitudinal study of adolescent brain development in the United States. Carina Heller and colleagues, publishing in npj Women’s Health in 2025, analyzed cortical brain measures in girls at the study’s four-year follow-up (average age 14). The 65 HC users in the sample, compared to 1,169 non-users, showed significantly thinner cortex in the bilateral paracentral gyrus, adjusting for pubertal stage and intracranial volume.⁵ A 2026 review in Biological Psychiatry: Global Open Science by Niamh MacSweeney, Adriene Beltz, Christian Tamnes, and colleagues synthesized the current evidence on adolescent HC use, brain structure, and depression risk. The authors concluded that despite the ubiquity of the exposure, its neurodevelopmental consequences remain poorly characterized in the mainstream literature, and that what is known is concerning.⁶
The manufacturers of the drugs have not been silent on the mood effects. The FDA-approved prescribing information for Yaz, Bayer’s drospirenone-containing combined oral contraceptive, lists mood changes (specifically: mood swings, depression, depressed mood, and affect lability) as an adverse reaction occurring in 2.2 percent of treated women in the pooled clinical trial dataset.⁷ The label for Yasmin, its predecessor, reports the same class of adverse reactions at 2.3 percent, with depression listed among the post-approval adverse events.⁸ These are the manufacturer’s own numbers, from the studies that supported the drug’s approval, and they represent the events serious enough to be captured as adverse reactions during short-term trials. The larger and more sustained effects that emerge across years of continuous exposure are not captured in the trial designs the FDA accepted.
The population-level evidence for the psychiatric consequences of long-term HC exposure is anchored in a 2016 Danish national registry study by Charlotte Skovlund, Øjvind Lidegaard, and colleagues, published in JAMA Psychiatry. The study followed more than one million Danish women aged 15 to 34 between 2000 and 2013.⁹ Women taking combined oral contraceptives had a 23 percent increased rate of first-time antidepressant use compared to non-users. Adolescents on the same drug had nearly double the rate of antidepressant initiation. Progestin-only formulations, hormonal IUDs, and non-oral formulations produced higher risks than the standard combined pill. A follow-up study by the same team, published in the American Journal of Psychiatry in 2018, extended the analysis to suicide and reported that adolescent women on HC were particularly vulnerable, with elevated risks for both suicide attempt and completed suicide.¹⁰
The Danish data is the largest and cleanest available. It is national, prospective, and controlled for prior psychiatric history. It has been available for a decade. Nothing in the diagnostic apparatus’s handling of the adult female ADHD wave acknowledges its existence.
The State the Drug Produces
A woman who has been on the pill for a decade or more is in a specific biological state. Her ovarian cycling has been suppressed through the years her prefrontal cortex was completing its maturation. Her endogenous estrogen has been replaced with a synthetic analog that binds dopamine-modulating receptors differently, and her endogenous progesterone with a synthetic progestin that does not produce the GABA-modulating metabolite her mood and stress responses depend on. She does not typically feel well.
What she reports, when a clinician takes any time beyond the ten-minute appointment to listen, is a specific cluster. She cannot focus on tasks that used to be easy. She loses her train of thought mid-sentence. She reads a page and cannot remember what she just read. She opens a browser tab and forgets why she opened it. She feels a fatigue that sleep does not touch. Her libido is absent in a way she has stopped noticing. Her mood is flat or unstable. She is anxious in social situations that used to be routine, and she cannot muster the drive that would once have carried her through work she found engaging. She is either sleeping too much or not enough, either eating too much or too little. She looks at her own life and cannot understand why she is not managing it well.
If a clinician were to hold that description against the DSM-5 diagnostic criteria for adult attention-deficit/hyperactivity disorder, most of the boxes would tick. Difficulty sustaining attention: yes. Loses things needed for tasks: yes. Easily distracted by extraneous stimuli: yes. Forgetful in daily activities: yes. Fails to give close attention to details: yes. The criteria are behavioral. They require no biological finding and no consideration of what medications the woman is taking or has been taking for the last fifteen years. A woman on HC who presents at 32 with this cluster meets the diagnostic threshold for adult ADHD as the DSM-5 has written it.
The DSM does not distinguish between executive dysfunction produced by an ongoing pharmacological exposure and executive dysfunction that would exist in the woman’s absence. One version requires a clinician to ask what she has been taking. The other version requires a clinician to write a prescription for a stimulant. The reimbursement system rewards the second and does not require the first.
The Diagnostic Capture
Between 2020 and 2022, new ADHD diagnoses in American women aged 23 to 29 nearly doubled, from 0.48 percent to 0.94 percent of the age-group population. New diagnoses in women aged 30 to 49 nearly doubled over the same period, from 0.34 percent to 0.66 percent. The doubling in the 18 to 22 group was of the same order: 0.55 to 0.98 percent.¹¹ The analysis, conducted by Epic Research on more than three million patient records, is not itself contested. What is contested is what caused it.
The mainstream explanations include the pandemic, the expansion of telehealth, the rise of ADHD content on social media, and the belated recognition of the inattentive presentation that predominates in women. Each captures something real. None of them explains why the biology of a disorder that the diagnostic literature classifies as neurodevelopmental and present from childhood would appear specifically in women whose adolescent and early-adult neurodevelopment took place on synthetic hormones.
A biological disorder present from childhood does not double in three years in the adult women of one country. What doubles in three years is a diagnostic category being applied to a population that meets its criteria for reasons the category was not designed to capture. The women being newly diagnosed at 32 do have the symptoms. The question the diagnostic apparatus is refusing to ask is what is producing them.
The doubling coincides with the fact that women in this age band are the first cohort in history who came of reproductive age on the modern low-dose combined oral contraceptive introduced in the 1990s, and continued that exposure into their thirties. Hormonal contraception is one of the most heavily prescribed classes of drug given to American women of reproductive age. Approximately 11 percent of all American women aged 15 to 49 currently take the pill, and a further 10.5 percent use hormonal IUDs or implants, with use concentrated in the reproductive years and especially in the 20 to 39 age band.¹² The typical prescription pattern begins in adolescence for acne, dysmenorrhea, or cycle irregularity, sustained through college and into early careers, often uninterrupted for a decade or more. The woman being newly diagnosed at 32 has, in most cases, spent a substantial portion of her adolescent and adult life on some form of the drug.
The corresponding stimulant prescription data is unambiguous. In 2022, for the first time in recorded history, American women surpassed men in dispensed stimulant prescriptions. Overall stimulant dispensing rose 57.9 percent between 2012 and 2022. The largest increases were concentrated in adult women, particularly those aged 30 to 40.¹³ A 2025 JAMA Psychiatry paper by Compton and colleagues at the National Institute on Drug Abuse documented, using pharmaceutical databases that capture 93 percent of American outpatient prescriptions, that stimulant prescriptions among women aged 35 to 64 rose from 1.2 million in the first quarter of 2019 to 1.7 million in the fourth quarter of 2022. That is a half-million-woman increase in less than four years, concentrated in the age band composed almost entirely of the exposed HC cohort. Wilson Compton, the study’s senior author and NIDA’s deputy director, told NBC News that the increase “is a very large increase that I can’t fully explain.”¹⁴ Ninety percent of dispensed stimulant prescriptions in the same period were written for ADHD. The male-female ADHD diagnostic ratio, which had run at 133 percent male excess in 2010, had collapsed to 28 percent by 2022, a nearly fivefold reduction of the gap in twelve years.¹¹
The diagnostic and pharmaceutical infrastructure that captured this population was built for a different one. The DSM adult ADHD criteria, the pharmaceutical marketing directed at adult women, the advocacy organizations that funnel adult women into diagnosis, and the telehealth companies that flooded the market during and after the pandemic (Cerebral being the most visible before its DEA investigations, but not the only one) share a common feature. None of them ask the newly diagnosed woman what medications she has been on and for how long. The diagnostic protocol that would identify HC exposure as the relevant variable in her presentation is not the diagnostic protocol that any of these platforms use.
Reimbursement structures follow the same logic. A stimulant prescription for adult ADHD is covered. A comprehensive endocrine workup with a discontinuation trial to determine whether the woman’s executive dysfunction resolves off HC is not. Cost and clinician time push the encounter toward the reimbursable outcome, which is the diagnosis and the stimulant prescription.
The Second Drug
What the stimulant does to a woman whose dopamine has been chronically suppressed by ten to fifteen years of HC exposure is not something the FDA has ever required to be studied. The drug is prescribed, and its short-term effect is what a stimulant does. It raises synaptic dopamine and norepinephrine. The woman feels she can think again. What she is experiencing is pharmacological compensation for the neurotransmitter suppression the first drug produced, not correction of an inherent brain disorder.
The pharmacology, the Schedule II status, the growth suppression in children, the cardiovascular warnings, the psychiatric adverse effect profile, and the withdrawal syndrome that follows discontinuation of stimulants are all documented in the FDA-approved prescribing information for Ritalin, Concerta, Adderall XR, and Vyvanse. That documentation is developed at length in the companion essay “What Is ADHD?”¹⁷ and in “The Arithmetic Pill”¹⁸ and is not re-argued here. What matters in this essay is what a Schedule II stimulant does on top of a HC-suppressed brain, and what the two drugs together look like as a pharmacological system.
Peter Breggin’s brain-disabling principle, articulated across four decades of psychiatric practice and most recently in his 2015 paper in Ethical Human Psychology and Psychiatry, states that psychiatric drugs work by producing a partial disability of brain function that the evaluator values.¹⁶ Applied to this system, the principle predicts that the stimulant will not restore the woman to what she was at fifteen before either drug was introduced. It will produce a different disability, layered on top of the disability the first drug produced, which the evaluator (and often the woman herself) will value because it feels like function. Focus becomes possible again. Task completion becomes possible again. What she loses (appetite regulation, sleep architecture, cardiovascular stability, and the emotional range that dopamine-suppressed and now dopamine-agonized systems no longer support) is documented on the stimulant label but not attributed to the drug. It is attributed to her ADHD.
The combined exposure has never been characterized in an FDA-required American clinical trial. There is no controlled study of adult women on continuous HC given stimulants for ADHD-type symptoms. What has been characterized, in the Swedish national registers, is the co-occurrence. Lundin and colleagues at Uppsala University and the Karolinska Institutet, publishing in the Journal of the American Academy of Child and Adolescent Psychiatry in 2023, linked registers covering 29,767 girls and young women aged 15 to 24 with an ADHD diagnosis and 763,146 without. In the ADHD cohort, 86.7 percent had also filled a stimulant prescription. When the same team examined the interaction between HC use and the underlying diagnosis, they found that ADHD acted as a significant effect modifier: young women with ADHD on combined oral contraceptives had over five times the depression risk of women without ADHD who were not on HC.¹⁵ The two drugs are prescribed independently by clinicians in different specialties who do not communicate. In the registry data, the intersection produces exactly the adverse outcome the mechanism section of this essay would predict.
What she is being told is that her brain is broken. What is actually happening is that her brain has been chronically exposed to one class of pharmacological agent that produces documented executive dysfunction, and is now being chronically exposed to a second class of pharmacological agent that partially compensates for the first. The compensation adds a second layer of pharmacology without repairing what the first produced.
The Loop
The loop, viewed from outside, is not accidental. Its components are prescribed by different clinicians in different specialties, funded by different insurance line items, marketed by different arms of the pharmaceutical industry, and named by different diagnostic categories. Its cumulative effect is that a girl who takes her first birth control pill at 15 has, by 32, a substantial probability of being on a Schedule II stimulant for a diagnosis that would not have been available to her at 15 and would not have been considered at 25.
The loop is financially reinforcing at every stage. The pill generates decades of monthly prescriptions. The executive dysfunction it produces generates a stream of encounters with the primary care and psychiatric systems, each billable. The ADHD diagnosis, once assigned, generates the stimulant prescription, which generates monthly refills, dose adjustments, and the cardiovascular and psychiatric monitoring the labels recommend but which is often not performed. The withdrawal that follows any attempt to stop the stimulant produces symptoms resembling the original ADHD presentation, which is used to justify continuation.
No actor in the loop is required to see it as a loop. The gynecologist who wrote the HC prescription is not in the room when the psychiatrist writes the Adderall prescription fifteen years later. The pharmaceutical companies that manufacture the two drugs are frequently the same corporate parent, and none of them has an incentive to fund the study that would establish the causal connection between their products.
The exposed cohort is now visible in the aggregate data: a decade of doubling in adult female ADHD diagnoses, a ratio collapse in male-to-female diagnostic rates, and women surpassing men in stimulant prescriptions for the first time in the history of American medicine. Each of these facts is present in the establishment’s own data. What is absent, at the establishment level, is any framework that would connect them.
The adult female cohort in the doubling has not come to the HC exposure with a neutral baseline. Many of the women being newly diagnosed at 32 were vaccinated in early childhood through the expanded American schedule the companion essay traced through its aluminum-locus coeruleus mechanism.¹⁷ The HC exposure of adolescence layers onto a nervous system that has already been chronically exposed. The two injuries compound rather than compete.
The first drug produces the state. The apparatus captures the state as a diagnosis. The second drug is prescribed for the diagnosis. The loop closes and the woman is inside it.
The Daughter
Somewhere in America or Britain or Australia today, a pediatrician is preparing to write a fifteen-year-old girl her first prescription for hormonal contraception. The reason may be acne. It may be irregular cycles. It may be dysmenorrhea. It may be the mother’s own request, based on what she has come to accept as the standard of care.
The mother is in the room. She has read this essay. She knows what the pediatrician is proposing and what a decade of the drug does to a brain that is not finished developing. She knows that her daughter’s prefrontal cortex will not complete its maturation until the late twenties. She knows what the Danish registry shows about adolescent women on this class of drug. She knows what the ABCD Study has documented about cortical thickness in the girls who took the first prescription. She knows the doubling in adult female ADHD diagnoses in the generation of women who came of age on this drug, and she knows that the doubling is her own generation.
She asks the pediatrician what non-hormonal options exist for the presenting problem. She asks what the natural course of adolescent cycle irregularity is. She asks whether the pediatrician has read the Skovlund papers, or the Gilfarb papers, or the Heller ABCD analysis. She asks what the discontinuation protocol would be if her daughter took the drug for a year and wanted to know what her body was actually like off it. The pediatrician will not have most of the answers.
The mother may consent to a short course. She may consent to none. What she has now, that she did not have at 15 or 25 or 32, is the framework to make the choice knowingly. She will say no where her own mother did not know to say no, and her daughter’s next fifteen years will not include the pathway her own did.
How to Explain It to a Six-Year-Old
A young woman took a pill every day for a long time. The pill told her body to be very quiet. Her body got very quiet, and stayed that way for many years.
After she had taken the pill for a long time, her brain got tired. She could not think as well as she used to. She could not remember what she was doing. She felt sad and worried, and she did not know why.
A doctor gave her another pill. The second pill told her brain to wake up. Her brain woke up and she could think again. But she was hungry in a wrong way, and she could not sleep, and her heart beat too fast.
She wondered why she needed two pills. She wondered why the first pill had told her body to be quiet in the first place. She wondered what she would be like if her body were allowed to be loud.
One day she stopped taking the first pill. Slowly, over months, her body woke up on its own. Her thinking came back. Her mood came back. She stopped needing the second pill too.
She thought about the girl she had been at fifteen, when the first pill was given to her. Nobody had told her what the pill would do. Nobody had told her, and nobody had known, because nobody had wanted to study it.
She decided she would tell her own daughter, when the time came.
In Print
The Unbekoming library is available in paperback, printed to order through Lulu and shipped worldwide. The shelf begins with the paradigm question underneath everything else — No Virus, the isolation problem, the collapse of virology’s foundational claims, and a disease-by-disease reappraisal — and moves through the suppressed compounds mainstream medicine set aside: The DMSO Book, Chlorine Dioxide: The Forbidden Remedy, The Iodine Book, and The Hydrogen Peroxide Book. Two more recover what’s still on the kitchen shelf: Baking Soda and The Castor Oil Book. Two more recover the minerals modern soil, water, and processing quietly stripped from the diet: The Magnesium Handbook and The Boron Book. Sitting alongside these is No Contagion, co-authored with Jamie Andrews — the case against germ theory itself, catalogued through 258 failed contagion experiments.
The critique books cover what medicine, dentistry, psychiatry, and veterinary practice have become. The Unvaccinated treats the completely unvaccinated as a comparison group across twenty chapters and five appendices. Medicalized Motherhood follows a woman through 123 documented interventions from teenage pill to postpartum discharge. Drilling for Profit treats cavities, gum disease, and crooked teeth as the dietary problem they are. What Your Vet Can’t Tell You applies the same critique to pets. Escape from Psychiatry documents the fabrication of the DSM and the specific damage of every major psychiatric drug class. The Vitamin K Injection covers what happens in the first hours of a newborn’s life.
The full shelf is at lulu.com/spotlight/unbekoming. A physical book reaches the person a Substack post never will — the skeptical relative, the friend who won’t click a link but might open a book, the visitor whose eye lands on a coffee table. Buy one to keep, and one to give away.
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References
Hill, S. E. (2019). This Is Your Brain on Birth Control: The Surprising Science of Women, Hormones, and the Law of Unintended Consequences. Penguin Random House / Avery.
Hill, S. E. and colleagues have published across multiple journals on hormonal contraceptive effects on the HPA axis and cortisol response. See also Mengelkoch, S. & Hill, S. E. (2023). Reviews of the stress-response and cognitive literature. Related work: Frokjaer, V. G. (2020). “Pharmacological sex hormone manipulation as a risk model for mental disorders.” Journal of Neuroscience Research, 98(4), 719-726.
Gilfarb, R. A., Ranade, S., Dybas, E., Biddle, A., Stewart, M., Rajesh, A., Leuner, B. & Lenz, K. M. (2025). “Hormonal contraceptives in adolescence impact the neuroimmune environment of the medial prefrontal cortex and hippocampus in female rats.” Brain, Behavior, and Immunity, 127, 315-328. doi:10.1016/j.bbi.2025.02.016.
Gilfarb, R. A., Ranade, S., Smail, M., Wangler, L., Stewart, M., Rajesh, A., Lenz, K. M. & Leuner, B. (2025). “Hormonal contraceptives during adolescence impact the female brain and behavior in a rat model.” Hormones and Behavior, 171, 105725. doi:10.1016/j.yhbeh.2025.105725.
Heller, C. et al. (2025). “Hormonal contraceptive intake during adolescence and cortical brain measures in the ABCD Study.” npj Women’s Health. Analysis of 65 HC users and 1,169 non-users at the ABCD Study’s four-year follow-up (average age 14).
MacSweeney, N., Dumoulin, T., Aksnes, E. R., Barth, C., Crestol, A., Heller, C., Nordeng, H., Toenders, Y. J., Winkler-Crepaz, K., Pletzer, B., Beltz, A. M. & Tamnes, C. K. (2026). “Adolescent Hormonal Contraceptive Use in the Context of Brain Development and Depression Risk: A Review and Considerations for Future Research.” Biological Psychiatry: Global Open Science, 6(5), 100758. doi:10.1016/j.bpsgos.2026.100758.
Yaz (drospirenone and ethinyl estradiol tablets), NDA 021676. FDA-approved prescribing information. Bayer HealthCare Pharmaceuticals Inc. Latest revised version accessible via FDA.gov/drugsatfda.
Yasmin (drospirenone and ethinyl estradiol tablets), NDA 021098. FDA-approved prescribing information. Bayer HealthCare Pharmaceuticals Inc. Latest revised version accessible via FDA.gov/drugsatfda.
Skovlund, C. W., Mørch, L. S., Kessing, L. V. & Lidegaard, Ø. (2016). “Association of Hormonal Contraception With Depression.” JAMA Psychiatry, 73(11), 1154-1162. doi:10.1001/jamapsychiatry.2016.2387.
Skovlund, C. W., Mørch, L. S., Kessing, L. V., Lange, T. & Lidegaard, Ø. (2018). “Association of Hormonal Contraception With Suicide Attempts and Suicides.” American Journal of Psychiatry, 175(4), 336-342. doi:10.1176/appi.ajp.2017.17060616.
Russell, J., Franklin, B., Piff, A., Allen, S. & Barkley, E. (2023). “Number of ADHD Patients Rising, Especially Among Women.” Epic Research, analysis of 3,389,383 patient records diagnosed with ADHD 2010–2022. Published 30 March 2023.
Daniels, K. & Abma, J. C. (2025). “Current Contraceptive Status Among Females Ages 15–49: United States, 2022–2023.” NCHS Data Brief No. 539, National Center for Health Statistics, Centers for Disease Control and Prevention.
IQVIA (2023). “Stimulant Prescription Trends in the United States from 2012 to 2023.” Report commissioned by the U.S. Drug Enforcement Administration Diversion Control Division. Available at deadiversion.usdoj.gov.
Compton, W. M., Han, B., Blanco, C., Johnson, K. & Jones, C. M. (2025). “Prescription Stimulant Use, Misuse, and Use Disorder Among US Adults Aged 18 to 64 Years.” JAMA Psychiatry, published online March 19 2025. doi:10.1001/jamapsychiatry.2025.0054. Analysis of 2019–2022 IQVIA Total Patient Tracker and National Prescription Audit databases and 2021–2022 National Surveys on Drug Use and Health.
Lundin, C., Wikman, A., Wikman, P., Kopp Kallner, H., Sundström-Poromaa, I. & Skoglund, C. (2023). “Hormonal Contraceptive Use and Risk of Depression Among Young Women With Attention-Deficit/Hyperactivity Disorder.” Journal of the American Academy of Child and Adolescent Psychiatry, 62(6). doi:10.1016/j.jaac.2022.07.847. Linkage of Swedish national registers covering 29,767 girls and young women with ADHD aged 15–24 and 763,146 controls.
Breggin, P. R. (2015). “Rational Principles of Psychopharmacology for Therapists, Healthcare Providers and Clients.” Ethical Human Psychology and Psychiatry, 17(3), 198-207.
Unbekoming. “What Is ADHD? An Essay on the Making of a Childhood Disease.” Lies are Unbekoming, Substack.
Unbekoming. “The Arithmetic Pill.” Lies are Unbekoming, Substack.
Unbekoming, you need to get this in front of Dr Chandler Marrs and her Hormones Matter site! You continue kicking serious academic ass with your posts!