Testosterone in Menopause: What We Know, What We Don't, and Why the FDA Is Asking Questions9/8/2026  Why testosterone in menopause is receiving so much attention Women are asking increasingly direct questions about testosterone in menopause:
The timing is significant. On September 17, 2026, the FDA Office of Women’s Health and Center for Drug Evaluation and Research will hold a public workshop titled “Testosterone Use in Menopausal Women.” The hybrid workshop will examine current evidence and knowledge gaps involving sexual function, cognition, mood, musculoskeletal health, testosterone measurement, monitoring, and long-term cardiovascular and breast safety. The FDA is not announcing approval, rejection, or a crackdown. It is asking where the evidence is strong, where it remains uncertain, how treatment should be studied and monitored, and what research is still needed. Women make testosterone tooTestosterone is not exclusively a male hormone. Women produce testosterone through the ovaries and adrenal glands, as well as through peripheral conversion of androgen precursors in other tissues. Testosterone can act directly through the androgen receptor. It can also be converted into other active hormones, including dihydrotestosterone and estradiol. These pathways help explain why testosterone has biologic relevance to female sexual physiology and other body systems. Men do not own testosterone, and women do not own estrogen. Both sexes produce multiple sex steroids, although concentrations, metabolism, and physiologic effects differ. Watch our full Testosterone + Menopause educational video. Book an appointment to discuss your symptoms, prior testing, and next steps with Lakeline Wellness.  Female androgen physiology diagram showing ovarian and adrenal production, peripheral conversion, and the shared biology of sex hormones. The graphic is educational and does not imply that hormone therapy is automatically indicated. Does menopause automatically cause testosterone deficiency? No. Menopause involves a major change in ovarian estrogen and progesterone production. Testosterone does not necessarily follow the same pattern or decline abruptly in every woman during the menopausal transition. Testosterone levels are influenced by age, ovarian function, adrenal androgen production, prior ovarian surgery, medications, binding proteins, and individual physiology. Women who undergo bilateral oophorectomy may experience a more abrupt reduction in ovarian androgen production than women undergoing natural menopause. That distinction matters. There is also no universally accepted serum testosterone concentration that independently diagnoses a female testosterone-deficiency syndrome. A low laboratory value and a clinical syndrome are not automatically the same thing. Where testosterone therapy has the strongest evidence The strongest evidence for systemic testosterone therapy in women concerns appropriately selected postmenopausal women with hypoactive sexual desire disorder, or HSDD. The 2019 Global Consensus Position Statement and the 2021 International Society for the Study of Women’s Sexual Health guideline conclude that testosterone may provide a moderate improvement in sexual function for this population when transdermal therapy is used at physiologic doses. This does not mean testosterone has been proven to improve every symptom associated with menopause. There is a large difference between saying testosterone has an evidence-supported role in selected women with HSDD and saying testosterone is a general treatment for fatigue, brain fog, weight gain, mood changes, or aging. What HSDD actually means HSDD is not simply a reduction in libido compared with an earlier period of life. It refers to persistent or recurrent low sexual desire associated with clinically meaningful personal distress after appropriate evaluation. Desire is affected by multiple factors. A careful assessment may consider:
A testosterone concentration does not diagnose HSDD. You diagnose the patient, not the testosterone number. Where claims may exceed the evidence Testosterone has biologic roles in multiple tissues. That does not establish that testosterone therapy improves every symptom associated with those tissues. Current evidence is strongest for sexual function in appropriately selected women with HSDD. Evidence for energy, mood, memory, cognition, brain fog, bone health, muscle mass, body composition, weight loss, metabolic health, general well-being, and anti-aging is variable, limited, or insufficient for routine treatment recommendations. The distinction is important: > Plausible physiology is not the same thing as demonstrated clinical benefit. Mechanistic research may explain why an intervention could work. Controlled human trials help determine whether it produces a meaningful outcome in the population studied. “Not proven” is also not identical to “proven not to work.” Where evidence is limited, the appropriate conclusion is uncertainty, not certainty in either direction.  Outcome-by-outcome evidence map using cautious tiers rather than promotional or dismissive labels. HSDD is shown as the best-supported indication; other outcomes are identified as variable, limited, or lacking sufficient long-term data. Why one testosterone number is not enough Testosterone testing in women is technically difficult because concentrations are relatively low and some commonly used assays are less reliable at female levels. Interpretation may involve:
Oral estrogen can increase SHBG, which may alter the amount of circulating testosterone that is available to tissues. Thyroid conditions and metabolic physiology can also affect binding proteins and interpretation. Current guidance does not support using total testosterone alone to diagnose HSDD. A baseline measurement may provide context, while follow-up testing can help determine whether treatment is producing physiologic or supraphysiologic exposure. The testosterone number may be more useful for monitoring exposure than for deciding, by itself, whether a woman needs treatment.  Laboratory interpretation diagram separating what testing can help assess, baseline context and treatment exposure, from what it cannot determine alone, whether a patient has HSDD or requires therapy.
Dose and formulation matter Physiologic female testosterone exposure and supraphysiologic androgen exposure are not the same therapeutic situation. The evidence base primarily involves non-oral, particularly transdermal, therapy designed to maintain testosterone within the physiologic premenopausal range. More testosterone is not necessarily better. Excess exposure can produce androgenic effects such as acne, increased facial or body hair, scalp hair loss in susceptible women, voice changes, or other virilizing effects. These effects are not reasons to sensationalize treatment, but they are reasons to use an appropriate dose and monitor clinically. Physiologic does not mean unlimited. Hormones work because dose matters. There is currently no FDA-approved systemic testosterone formulation specifically approved for women in the United States. Clinicians may use appropriately reduced doses of approved male formulations off-label. Some clinicians and patients also encounter compounded preparations. Compounded products are not automatically identical in quality or automatically unsafe. However, professional guidance has raised concerns about consistency, reproducibility, and the limited efficacy and safety data available for compounded testosterone. The formulation, dose, source, and monitoring plan should be discussed explicitly. Oral testosterone has raised greater concern about lipid effects and is not the route on which the strongest contemporary evidence is based. Pellets and injectable formulations may also produce less predictable or excessive exposure and are not supported by the same evidence as carefully dosed transdermal therapy. What we know, and do not know, about long-term safety Short-term studies of physiologic-dose, non-oral testosterone have generally not identified serious safety signals in appropriately selected women. Acne and increased hair growth are among the more consistently reported adverse effects. That is not the same as proving lifelong safety. Long-term cardiovascular, breast, metabolic, ovarian, and endometrial safety remain incompletely characterized. Many studies were relatively short and excluded women with substantial baseline cardiovascular or metabolic risk. We have useful short-term safety information, but the quality and duration of long-term data are not sufficient to make sweeping statements about lifelong cardiovascular or breast safety. Testosterone has not been proven to cause cardiovascular disease or breast cancer. It has also not been proven completely free of those risks. Identifying uncertainty should not frighten patients. It should make clinical decision-making more scientifically honest. Testosterone does not exist in isolation Consider a 55-year-old woman with decreased libido, fatigue, weight gain, reduced muscle mass, poor sleep, mood changes, and brain fog. Someone tells her, “You need testosterone.” That conclusion is premature. An appropriate evaluation may consider sleep quality and sleep apnea, medications, thyroid physiology, metabolic health, insulin resistance, activity level, muscle mass, iron status, depression or anxiety, pain with intercourse, genitourinary syndrome of menopause, relationship factors, chronic stress, and, when clinically appropriate, relevant hormone testing. Not every patient needs every test. The point is diagnostic reasoning. Adding testosterone to a complicated endocrine picture does not make the endocrine picture less complicated. The same principle applies when distinguishing menopause symptoms from thyroid-related symptoms; see Menopause or Thyroid? How Austin Women Can Interpret Overlapping Symptoms. The two easy mistakes Mistake one: dismissing testosterone because it has traditionally been called a “male hormone.” That ignores female androgen physiology and the evidence supporting treatment for selected women with HSDD. Mistake two: assuming that because testosterone has biologic roles in women, giving more testosterone must improve every tissue containing an androgen receptor. That exceeds the available clinical evidence. There is a large space between those two positions, and that is where actual clinical medicine lives. What the FDA workshop may help clarifyThe September 17 FDA workshop may help define priorities for future research, including:
The related Federal Register docket, FDA-2026-N-5479, accepts public comments through October 19, 2026. The workshop itself is a scientific and regulatory discussion, not a treatment recommendation. Practical questions to discuss with your clinician If you are considering testosterone for women during or after menopause, ask:
For women in Austin, Cedar Park, and surrounding Central Texas communities, Lakeline Wellness provides individualized review of symptoms, health history, prior records, and appropriate diagnostic information through its Diagnostic & Functional Testing pathway. Patients who are unsure where to begin can review the new-patient process. Conclusion Testosterone matters to female physiology. The evidence also matters. For appropriately selected postmenopausal women with HSDD, systemic transdermal testosterone may provide a moderate improvement in sexual function. That evidence does not establish testosterone as a universal treatment for every symptom attributed to menopause. For women experiencing changes in libido, energy, body composition, mood, or other symptoms during menopause, testosterone may be one part of the clinical discussion, but it should not be considered in isolation from the rest of the endocrine and medical picture. A thoughtful evaluation can help determine which factors are actually contributing and whether hormone therapy is appropriate. Primary References
Disclaimer: This information is for educational purposes only and is not intended to diagnose or treat any medical condition. Please consult with a healthcare professional before starting any new supplement or dietary regimen. See our full disclaimers here.
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 If you are in your 40s or 50s and experiencing fatigue, brain fog, sleep disruption, weight change, mood shifts, or temperature intolerance, you may be asking: Is this menopause, a thyroid problem, or both? That question is clinically reasonable. Perimenopause and thyroid dysfunction can produce similar symptoms, but similar symptoms do not necessarily mean the same underlying mechanism. A careful evaluation considers menstrual history, thyroid physiology, medications, prior laboratory results, sleep, metabolic health, and other contributors rather than assigning every symptom to one explanation. 1. Why menopause and thyroid symptoms are so easily confused Perimenopause is the transitional period before the final menstrual period, when ovarian hormone production and menstrual cycles become more variable. Menopause is confirmed retrospectively after 12 consecutive months without menstruation when another cause is not responsible. The thyroid is an endocrine gland in the neck that produces hormones involved in energy use, temperature regulation, cardiovascular function, cognition, and gastrointestinal activity. Hypothyroidism means thyroid hormone production is insufficient. Hyperthyroidism means thyroid hormone activity is excessive. These systems are biologically different, but their symptoms can overlap. That overlap creates two common errors:
Neither conclusion is adequate without considering the full clinical pattern.  The overlap zone shows why fatigue, weight or body-composition changes, brain fog, sleep disruption, mood changes, hair and skin changes, temperature intolerance, and palpitations cannot identify the cause by themselves. The diagram is educational and not diagnostic. 2. What the new research found A recent study in the Journal of Clinical Endocrinology & Metabolism followed 7,644 Japanese women through natural menopause. The cohort included annual health-checkup data from 2004 through 2024, with a median follow-up of 13.7 years and 86,967 visits involving thyroid measurements. The researchers examined trajectories of thyroid-stimulating hormone, or TSH, and free thyroxine, or free T4, before and after natural menopause. The main findings were:
The practical message is important: > Thyroid problems become more common around menopause. That does not necessarily mean menopause caused the thyroid problem.  This timeline separates gradual aging-related thyroid trends from a distinct menopause-caused change. It also identifies what the study did and did not establish. The cohort was Japanese and based on generally healthy women receiving annual health checkups. 3. What the research does not prove The study is valuable, but it should not be overinterpreted. It does not prove that menopause never affects how a person feels. Menopausal physiology can produce substantial symptoms, including vasomotor symptoms, sleep disruption, sexual or genitourinary symptoms, and changes in mood or cognition. It does not prove that thyroid disease and menopause are unrelated. A person can enter perimenopause while also developing Hashimoto’s thyroiditis, Graves’ disease, medication-related thyroid changes, or another condition. It does not establish that the findings apply identically to every population. The cohort consisted of Japanese women who experienced natural menopause and excluded women using hormone replacement therapy or those with surgical menopause. Differences in genetics, medical care, nutrition, environmental exposures, medication use, and population characteristics may affect generalizability. Finally, the study does not make symptoms diagnostically specific. Laboratory trends must still be interpreted in the context of the individual patient. 4. The common symptoms that overlap The most frequent overlap occurs with:
The symptom is real even when its cause is uncertain. The clinical task is to identify the most coherent explanation, not to force every symptom into one category. 5. How thyroid function is evaluated A thyroid evaluation commonly begins with TSH, a pituitary hormone that signals the thyroid to produce thyroid hormone. TSH is a sensitive initial test, but it is not interpreted in isolation. Depending on the result and clinical context, evaluation may include:
A laboratory reference interval answers one question: whether a result falls within the statistical range established by that laboratory. It does not answer every clinical question. At the same time, a high-normal or low-normal value does not automatically require treatment. 6. How menopausal physiology is evaluated For most women in the expected age range, perimenopause is evaluated primarily through:
Estradiol, progesterone, and androgen testing may be considered in selected situations. However, ovarian hormone levels can fluctuate substantially during perimenopause. One isolated measurement may not fully characterize the transition or explain symptoms. Urinary steroid hormone metabolites may provide additional information in selected patients, particularly when a clinician is evaluating broader hormone metabolism patterns. They should not be represented as a stand-alone test that diagnoses menopause or independently explains every symptom. The clinical question determines whether testing is useful. More testing is not automatically better testing. 7. Why thyroid autoimmunity is a separate issue Hashimoto’s thyroiditis is an autoimmune condition in which immune activity targets thyroid proteins, commonly reflected by TPO or thyroglobulin antibodies. Graves’ disease is an autoimmune cause of hyperthyroidism involving antibodies that stimulate the TSH receptor. This distinction is essential: > Autoimmunity and thyroid hormone production are related questions. They are not identical questions. A person may have positive thyroid antibodies while TSH and free T4 remain normal. Antibodies may indicate autoimmune susceptibility or thyroid autoimmunity, but they do not by themselves establish that thyroid hormone production is currently abnormal or that treatment is required. Conversely, thyroid dysfunction can occur without the antibody pattern expected in a particular autoimmune disease. Antibodies help clarify cause; TSH and free T4 primarily assess current thyroid function. 8. Other conditions that can mimic either problem A complete differential may also consider:
This is not an exhaustive checklist. The appropriate evaluation depends on the symptom pattern, age, menstrual history, examination, medications, and previous results. 9. When a more complete evaluation may be appropriate A broader assessment may be reasonable when symptoms are persistent, disproportionate, or not explained by the menstrual pattern alone. It may also be appropriate when symptoms begin unusually early, thyroid disease runs in the family, there is a history of autoimmune disease, or previous thyroid tests have changed over time. Very heavy or prolonged bleeding, fainting, chest pain, severe shortness of breath, a sustained rapid or irregular heartbeat, marked weakness, or sudden neurologic changes require timely medical evaluation. At Lakeline Wellness Center, Dr. Carsrud’s clinical thinking begins with the patient’s question, then connects symptoms with menstrual history, thyroid testing, medications, prior records, sleep, metabolic factors, and other relevant contributors. Patients can review the Diagnostic & Functional Testing service and Practitioners page. The Start Here pathway explains how to provide records and determine whether an initial consultation or testing-focused inquiry is the appropriate first step.  The pathway emphasizes that thyroid testing, menopause evaluation, and assessment of other contributors answer different questions. The goal is a coherent clinical picture rather than a single test or label.
10. Practical conclusion If you are asking “menopause or thyroid,” the most accurate answer may be: the symptoms overlap, and more than one physiologic process may be present. The 2026 JCEM study supports an important distinction. Thyroid abnormalities become more common as women age, but the menopausal transition itself did not appear to create a distinct clinically meaningful change in thyroid function in this large Japanese cohort. That finding should not dismiss menopausal symptoms or end the thyroid evaluation. It should encourage better reasoning. Human beings are allowed to have more than one thing wrong at the same time. A careful evaluation does not assume that every symptom is menopause, and it does not assume that every symptom is thyroid disease. It asks which systems are involved, what the available evidence shows, and what remains uncertain. If fatigue, brain fog, weight change, palpitations, or sleep disruption have been attributed to menopause but the explanation still does not seem complete, a more comprehensive evaluation may help determine which physiologic systems deserve closer attention. Primary References
Disclaimer: This information is for educational purposes only and is not intended to diagnose or treat any medical condition. Please consult with a healthcare professional before starting any new supplement or dietary regimen. See our full disclaimers here [https://www.lakelinewellness.com/disclaimers.html]. Book an appointment with Lakeline Wellness Center Postpartum OCD vs. Postpartum Psychosis: Why Postpartum Mental Health Is Not One Diagnosis8/25/2026  A mother has frightening thoughts after giving birth. Is this a common postpartum experience, postpartum depression, postpartum OCD, or a sign that she may be dangerous to herself or her baby? The answer depends less on the topic of the thought than on the person’s relationship to it. Is the thought unwanted and recognized as irrational? Or is it accepted as true, justified, or part of a command? That distinction can separate an intrusive obsession from a delusion and can change the level of urgency. Postpartum mental health is not one diagnosis “Postpartum mental health” describes a period of increased psychiatric vulnerability. It is not a diagnosis. Several conditions can occur after childbirth, and they are not interchangeable.  Postpartum conditions require different types of assessment. It is not a linear severity scale, and depression, anxiety, and OCD can still cause substantial impairment even when psychosis is absent.
A depression screening questionnaire can be useful, but it cannot by itself distinguish unipolar depression from bipolar disorder, OCD, or psychosis. The American College of Obstetricians and Gynecologists recommends screening during pregnancy and postpartum with systems in place for diagnostic assessment, treatment, monitoring, and follow-up. [1] Postpartum OCD intrusive thoughts versus postpartum psychosis The phrase “I am afraid I might hurt my baby” does not establish a diagnosis. The clinician must assess the nature of the thought, the person’s insight, emotional response, behavior, and overall mental state. Ego-dystonic intrusive thoughts in postpartum OCD An ego-dystonic thought is inconsistent with a person’s values and sense of self. In postpartum OCD, a mother may experience a vivid, unwanted image of accidentally dropping the baby or intentionally causing harm. The thought may be horrifying to her. She may say, “I would never do that,” avoid knives or bathtubs, repeatedly check the baby, or ask others for reassurance. The distress is generated by the presence of the thought and what she fears it might mean. She generally recognizes the thought as excessive, irrational, or symptomatic. This is called retained insight. An intrusive obsession is not the same as intent. Ego-dystonic harm thoughts, by themselves, do not mean that a mother wants to act on them. However, postpartum OCD still deserves timely assessment and treatment, particularly when avoidance, compulsions, depression, or inability to function are present. [3] Delusions and impaired reality testing in postpartum psychosis A delusion is a fixed belief that is not supported by reality and is held despite evidence to the contrary. In postpartum psychosis, a mother may believe that the baby is possessed, that family members are trying to poison the infant, or that she has a special mission requiring a particular action. Hallucinations may also occur, including voices or commands. The central concern is impaired reality testing. The person may believe the perception or idea is true, justified, or necessary. Insight may be poor or absent. Severe confusion, disorganization, rapidly changing mood, and inability to sleep can accompany the psychosis. The topic of the thought can be similar in OCD and psychosis. The clinical distinction is the person’s relationship to the thought.  The same surface topic can represent different syndromes. OCD is characterized by intrusive thoughts with preserved insight; psychosis involves delusions or hallucinations with impaired reality testing. Safety comes before physiological investigation Psychosis, mania, suicidal intent, impaired reality testing, or danger to the mother or child requires immediate psychiatric and medical assessment. Seek emergency help now if a postpartum person:
Call 911, go to the nearest emergency department, or call or text 988 for the Suicide & Crisis Lifeline. Do not leave a person with suspected psychosis alone with the infant. Involve a trusted support person and communicate clearly that the situation requires urgent professional evaluation. Bipolar-spectrum illness also must be considered. ACOG recommends bipolar screening before pharmacotherapy for depression or anxiety when bipolar history has not already been assessed. In a person with unrecognized bipolar illness, antidepressant monotherapy can worsen mood instability or precipitate mania in some cases. Medication decisions, particularly during breastfeeding, should be made with an appropriately qualified clinician and coordinated psychiatric care. [1, 2] A psychiatric diagnosis does not end the medical investigationA psychiatric diagnosis is a syndrome label. It describes a recognizable constellation of symptoms, but it does not necessarily explain every factor contributing to vulnerability. After immediate safety has been addressed, conventional medical evaluation may consider medication effects, substance exposure, infection, anemia, endocrine disease, neurologic conditions, autoimmune encephalitis, delirium, and other causes when clinically indicated. Postpartum psychosis can resemble or coexist with medical illness, which is one reason urgent evaluation should include both psychiatric and medical assessment. [4] Relevant physiologic domains may include:
 Psychiatric safety assessment first, conventional medical differential second, and additional physiologic context third. It explicitly communicates that no single laboratory or specialty test diagnoses postpartum psychiatric illness. HRV assessment, stool testing, urinary hormone-metabolite testing, and urinary neurotransmitter testing should not be used to diagnose postpartum psychiatric illness. If considered at all, they are additional physiologic information after appropriate psychiatric risk assessment and conventional medical evaluation. They cannot replace a mental-status examination, suicide-risk assessment, emergency care, or psychiatric treatment. For related discussions of autonomic regulation, readers can review Lakeline’s educational article on the wired-and-tired brain and autonomic dysregulation. Questions about testing can be reviewed through Lakeline’s Diagnostic and Functional Testing service, with the understanding that test selection must follow the clinical question. Practical next steps If symptoms are present but there is no immediate danger:
 The clinical sequence: immediate safety check, urgent evaluation when indicated, bipolar screening before antidepressant monotherapy, and thoughtful medical follow-up. It is educational and does not replace clinical judgment.
Complex postpartum presentations deserve both appropriate psychiatric assessment and thoughtful medical evaluation. Learn more about Dr. Carsrud’s approach to complex clinical cases at Lakeline Wellness. New patients can review Start Here to understand the practice and available care pathways. Primary References
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Dr. N.D. Victor CarsrudFunctional Internist in the Trenches 
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