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Huberman Lab

Female Hormone Health, PCOS, Endometriosis, Fertility & Breast Cancer | Dr. Thaïs Aliabadi

with Dr. Thais Aliabadi

Published November 24, 2025
View Show Notes

About This Episode

Andrew Huberman and obstetrician-gynecologist Dr. Thais Aliabadi discuss how PCOS and endometriosis-two leading causes of infertility-are massively underdiagnosed and frequently dismissed as "normal" women's issues. They explain diagnostic criteria, underlying biology such as hypothalamic-pituitary-ovarian axis disruption and insulin resistance, and treatment options including lifestyle, supplements, medications, and surgery. They also cover egg count testing, egg freezing, endometriosis pain management, perimenopause and menopause symptoms, breast cancer lifetime risk assessment, and the need for women to actively advocate for their own health within a flawed medical system.

Topics Covered

PCOS Endometriosis Infertility Insulin resistance GLP-1 agonists Metformin Egg freezing Breast cancer risk assessment Perimenopause and menopause Women's health advocacy

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Quick Takeaways

  • PCOS and endometriosis are among the top causes of infertility worldwide, yet Dr. Aliabadi estimates over 90% of affected women are never correctly diagnosed or treated.
  • PCOS diagnosis requires any two of three criteria: high androgen symptoms, ovulation dysfunction (irregular periods), and PCOS-type ovaries or elevated AMH, and it can present in four different phenotypes.
  • Insulin resistance, chronic inflammation, and disruption of the brain-pituitary-ovary axis are core drivers of PCOS symptoms and must be treated, not just masked with birth control.
  • Endometriosis pain (painful periods, painful sex, bowel and bladder pain, chronic pelvic pain, bloating) is often normalized, but painful periods that disrupt life are not normal and strongly suggest endometriosis.
  • Endometriosis cannot be reliably ruled out by normal ultrasound or MRI; gold-standard diagnosis and treatment is laparoscopic excision by a properly trained surgeon.
  • Every young woman should know her egg count (AMH) and be screened for PCOS and endometriosis early, because both conditions can silently destroy egg quality and egg reserve.
  • Women with a lifetime breast cancer risk of 20% or more (by tools like Tyrer-Cuzick) should start breast imaging around age 30 and may qualify for enhanced screening or preventive treatments.
  • Because access, time pressure, and training gaps limit many clinicians, women must be strong self-advocates: arrive with specific requests (AMH, pelvic ultrasound, PCOS/endometriosis workup, risk calculators) and not accept dismissal of their symptoms.

Podcast Notes

Opening and framing of women's health problems

Cataract analogy and underdiagnosis of infertility causes

Comparison between cataract diagnosis and infertility diagnosis[0:00]
• Every ophthalmologist recognizes cataracts, the most common form of blindness, and missing the diagnosis would be rare.
• Dr. Aliabadi contrasts this with infertility: despite PCOS and endometriosis being leading causes, about 90% of women with these conditions are not diagnosed.
Women's symptoms are dismissed or normalized[4:09]
• She says women's symptoms are routinely dismissed, minimized, or labeled as anxiety or stress instead of being investigated.
• Conditions like PCOS, endometriosis, chronic pelvic pain, and infertility often underlie these symptoms but are left undiagnosed because no one listens.

Huberman introduces the guest and topics

Guest introduction[0:52]
• Andrew Huberman introduces himself as a professor of neurobiology and ophthalmology at Stanford.
• He introduces Dr. Thais Aliabadi as an obstetrician, gynecologist, surgeon, and sought-after expert and trusted voice in women's health.
Planned topics for the episode[1:01]
• They will discuss PCOS, endometriosis, breast cancer, perimenopause, and menopause, among other women's health issues.
• Huberman notes many physicians wrongly normalize pain, hair thinning, mood changes, and other symptoms instead of recognizing them as pathology.
• He says Dr. Aliabadi has created zero-cost online tools to help women assess risks for breast cancer, PCOS, and endometriosis.

Fertility, egg count, and the need for early screening

Typical fertility trajectory vs. reality with PCOS/endometriosis

Why "textbook" fertility curves are misleading[8:57]
• Huberman asks about the standard fertility curve (chances of pregnancy by age brackets) and how it matches real life.
• Aliabadi says she cannot simply reassure 20-year-olds that they're fine because undiagnosed PCOS and endometriosis can destroy egg count and quality early.
Women are born with a fixed egg reserve that declines over time[5:27]
• She explains women are born with millions of eggs and do not make more after birth.
• As women age, egg number decreases and quality also declines; by menopause, about 1,000 eggs remain.
Impact of PCOS and endometriosis on egg reserve[5:43]
• PCOS and endometriosis affect both egg count and egg quality.
• She has patients with endometriosis who by age 30 have zero eggs left due to ongoing, unaddressed disease.
• She mentions treating 13- and 14-year-olds with endometriosis, including a 14-year-old whose egg count resembles that of a 40-year-old.

Universal screening and AMH testing

Every young woman should be screened for PCOS and endometriosis[7:28]
• Aliabadi insists every girl on the planet should be screened for endometriosis, PCOS, and know her egg count.
• She argues that if every 20-year-old saw her once, she could "shut down fertility clinics" by preventing infertility through early diagnosis and treatment.
AMH blood test for egg count[7:39]
• AMH (anti-Mullerian hormone) is a simple blood test that reflects egg count and is covered by most insurances.
• She says even teenagers with severe pain who miss school for periods deserve an egg count check, and sometimes she freezes their eggs by age 16.

PCOS: definition, prevalence, and diagnostic criteria

What PCOS is and how common it is

Definition and prevalence[15:38]
• PCOS (polycystic ovary syndrome) is the most common hormone disorder in women of reproductive age.
• It affects about 15% of women in the U.S., and in some Middle Eastern countries prevalence exceeds 20%.
• Literature estimates 70% of PCOS cases go undiagnosed, but Aliabadi believes the real number is over 90%.
Birth control is only a small part of PCOS treatment[16:21]
• She criticizes the common practice of treating PCOS with birth control pills alone, saying that is only a tiny piece of an appropriate treatment plan.

Diagnostic criteria for PCOS

Rotterdam-style criteria: 2 of 3 needed[16:33]
• Criterion 1: Symptoms of high testosterone/androgens such as facial hair, body hair, acne, oily skin, or male-pattern hair thinning.
• Criterion 2: Ovulation dysfunction, manifested as irregular periods (cycles longer than ~35 days) or about eight periods per year.
• Criterion 3: PCOS-looking ovaries on ultrasound (numerous small follicles, often described as a "string of pearls").
• You only need two of these three criteria to be diagnosed; all three are not required.
Misconceptions about cysts and blood testosterone levels[16:37]
• PCOS does not mean actual cysts; the name is misleading and leads some doctors to wrongly rule out PCOS if they don't see cysts.
• In 2023 the "PCOS morphology" criterion was updated to include elevated AMH or elevated egg count as diagnostic evidence.
• You do not need a high testosterone blood level to qualify; clinical signs of androgen excess alone can satisfy that criterion.

Typical PCOS symptom cluster and mood issues

Common symptom pattern[19:16]
• Irregular periods, weight gain and difficulty losing weight, acne, hair loss, facial and body hair, and infertility are common in PCOS.
• She notes many women are repeatedly told to "eat less" and "exercise more" and that nothing is wrong.
Mood disorders, eating disorders, and PCOS[19:47]
• About 75% of PCOS patients gain weight; roughly 25% are lean but still have PCOS.
• A large proportion of her PCOS patients struggle with anxiety and depression and are described as "moody".
• She estimates 60-70% of her PCOS patients have disordered eating or full eating disorders.
• She believes many undiagnosed PCOS patients are inside eating disorder centers, where their metabolic drivers are not addressed.

PCOS in teenagers and the four phenotypes

Diagnosing PCOS in adolescents

Why teen diagnosis is tricky[23:17]
• Early cycles are normally irregular and young ovaries naturally have many follicles, making PCOS-like ultrasound findings less specific in teens.
• For teenagers, PCOS morphology on ultrasound and AMH levels should not be used diagnostically.
• Teen PCOS diagnosis should rely on irregular periods plus high-androgen symptoms, with caution about labeling but openness to treating.

Four phenotypes of PCOS and diagnostic confusion

Phenotype A: classic PCOS[29:35]
• Classic PCOS has all three: high androgen symptoms, ovulatory dysfunction, and PCOS morphology on ultrasound.
Phenotype B: hyperandrogenic with ovulatory dysfunction but normal ovaries[30:11]
• These women have high androgen symptoms and irregular ovulation but normal-appearing ovaries on ultrasound.
Phenotype C: ovulatory PCOS[30:23]
• These women have PCOS-looking ovaries and high androgen symptoms but apparently regular cycles.
• Even with regular bleeding, many of these women are not truly ovulating; the bleeding can be estrogen withdrawal rather than a true ovulatory cycle.
Phenotype D: non-hyperandrogenic PCOS[32:20]
• These women have ovulatory dysfunction and PCOS-like ovaries but no obvious androgen-excess symptoms.
• The diversity of phenotypes makes PCOS hard for many doctors to recognize, especially in lean women or those without acne/hirsutism.

PCOS pathophysiology: brain-ovary axis and insulin resistance

Normal hypothalamus-pituitary-ovary (HPO) axis

How a normal cycle works[34:40]
• Hypothalamus releases GnRH in pulses, stimulating pituitary FSH to recruit ovarian follicles.
• Growing follicle secretes estrogen; when estrogen is high for about 48 hours, pituitary releases LH, triggering ovulation.
• After ovulation, the corpus luteum secretes progesterone to stabilize the uterine lining for implantation.

What goes wrong in PCOS at the HPO axis

Altered GnRH pulsing and LH/FSH imbalance[37:32]
• In PCOS, GnRH pulses too rapidly, skewing the FSH-to-LH ratio: FSH drops and LH rises.
• High LH overstimulates theca cells in the ovary to secrete androgens.
• Excess androgens inhibit normal follicle maturation, "freezing" follicles so they don't ovulate, while still secreting estrogen at sub-peak levels.
• About 70-80% of PCOS patients do not ovulate; among those who do, many have poor egg quality or an inhospitable uterine environment.

Insulin resistance as a core PCOS driver

Basic explanation of insulin and insulin resistance[41:42]
• Carbohydrates are broken into glucose, which triggers insulin release from the pancreas.
• Insulin's job is to open channels in muscle and liver cells to move glucose from blood into cells for energy.
• Around 80% of PCOS patients have insulin resistance, often genetically driven, where cells do not respond properly to insulin.
Vicious cycles between insulin and androgens[43:52]
• Androgens generated in PCOS further worsen insulin resistance.
• When cells resist insulin, glucose stays in the blood, pushing the pancreas to release more insulin.
• High insulin directly stimulates the ovaries to produce more androgens and suppresses ovulation.
• Insulin also suppresses liver production of sex hormone-binding globulin (SHBG), increasing free testosterone and worsening acne, hair loss, and hirsutism.
• Insulin promotes conversion of excess glucose to triglycerides, which can be stored as visceral fat and as VLDL particles, raising cardiovascular risk.

Inflammation, visceral fat, genetics, and epigenetics in PCOS

Visceral fat and chronic inflammation[45:50]
• Visceral fat (around organs) secretes inflammatory cytokines, unlike subcutaneous fat under the skin.
• Inflammation worsens insulin resistance and stimulates ovaries to secrete more androgens, forming a reinforcing loop.
Genetic and epigenetic factors[49:47]
• PCOS frequently clusters in families with diabetes, prediabetes, gestational diabetes, or obesity on either parent's side.
• She cites the phrase: "Your genes load the gun; your environment pulls the trigger" to describe epigenetic influences like diet, stress, sleep, and exercise.
• Even with a strong genetic predisposition, healthy lifestyle can suppress expression of PCOS symptoms; poor lifestyle exacerbates them.

PCOS treatment strategies: lifestyle, supplements, metformin, GLP-1s, and fertility meds

Birth control's limited but real role

How birth control helps and why it's not enough[52:43]
• Combination pills increase SHBG and thus lower free testosterone, improving acne and hair symptoms and regulating bleeding.
• She notes many PCOS patients are moody and do not tolerate estrogen-containing birth control well, reporting more anxiety, depression, and appetite changes.
• She describes a progesterone-only pill (Slynd) as an option for androgen suppression without estrogen.

Lifestyle and supplement approaches to insulin resistance

Lifestyle: exercise, diet, sleep, stress[55:35]
• She emphasizes exercise, including walking 10-15 minutes after meals, to improve glucose handling.
• She recommends good sleep, low-inflammatory diets, and stress reduction to impact insulin resistance and inflammation.
Ovi online tool and supplement[1:07:27]
• Aliabadi created an online platform called Ovi (OVII.com) with an algorithm-based questionnaire to estimate PCOS likelihood.
• She developed a supplement (Ovi) containing inositol, vitamin D, coenzyme Q10, L-carnitine, wild mulberry leaf, and other ingredients to improve insulin sensitivity and inflammation.
• Mulberry leaf in the supplement can block about 40% of carbohydrate absorption from a meal when taken before it, according to her.
Specific supplements and rationale[1:03:35]
• Inositol (various forms) can increase insulin sensitivity and help regulate cycles and ovulation.
• Low vitamin D contributes to insulin resistance, so correcting deficiency is important.
• She mentions coenzyme Q10 and L-carnitine as potentially helpful for egg quality by reducing inflammation and supporting mitochondrial function.

Metformin and GLP-1 agonists in PCOS

Metformin dosing and effects[1:05:52]
• Metformin improves insulin sensitivity by helping cells take up glucose more effectively.
• She typically starts PCOS patients at 750 mg at night, then adds 750 mg in the morning if tolerated, and may go up to 1,000 mg twice daily.
• Common side effects are nausea and diarrhea; she suggests starting slowly and adding only if needed.
GLP-1 agonists (e.g., Trulicity) and weight loss[1:10:14]
• She began using GLP-1 agonists in 2014 for PCOS patients with insulin resistance and obesity, often seeing 50-100 lb losses.
• GLP-1s are not simply appetite suppressants; they regulate insulin, rapidly clear glucose from the blood, and improve insulin sensitivity.
• In her practice, four months of properly used GLP-1s results in an average 24 lb weight loss.
• Patients report feeling less inflamed and having a quieter brain with fewer intrusive food cravings.
• She notes GLP-1s also reduce cravings for alcohol and suggests they may be useful for some people with alcohol use problems.

Fertility treatment in PCOS

Use of letrozole and clomiphene[1:19:43]
• She uses letrozole or clomiphene (Clomid) to induce ovulation after improving insulin resistance.
• Letrozole induces ovulation in about 60-70% of PCOS patients; Clomid performs slightly less well.
• She has patients try naturally for six months (if over 35) or up to a year (if younger and egg count is good) before referring to fertility clinics.
Reframing AMH and egg count in PCOS[1:30:25]
• PCOS patients often have very high AMH and many follicles, but egg quality can be poor.
• She shares cases where 40-year-old women produce 30 eggs yet no embryos, indicating undiagnosed PCOS despite high egg numbers.
• Rule of thumb: each 0.1 AMH roughly equals one follicle; AMH of ~1 suggests about 10 follicles, while 0.5 at age 40 indicates about five follicles.

Endometriosis: definition, symptoms, and massive underdiagnosis

What endometriosis is and how it behaves

Definition and ectopic endometrial-like tissue[1:36:21]
• Endometriosis is when tissue similar to the uterine lining (endometrium) exists outside the uterus, on ovaries, bladder, bowel, or elsewhere.
• Each month, estrogen stimulates both the uterine lining and these ectopic implants; when the lining sheds as a period, the implants also bleed internally.
• This internal bleeding and inflammatory response cause pain and progressive scarring.
Prevalence and diagnostic delays[1:38:52]
• Official estimates suggest around 10% of women have endometriosis, but Aliabadi believes the real number is above 20%.
• On average in the U.S., it takes 9-11 years and visits to 5-10 doctors for a woman with endometriosis to be diagnosed.
• She has seen patients who have consulted up to 50 doctors before diagnosis.

Symptoms and self-diagnosis of endometriosis

Painful periods are not normal[1:39:54]
• She stresses that painful periods that disrupt life are not normal and should be treated as endometriosis until proven otherwise.
• Criteria she gives: if pain makes you miss school or work, stay in bed, change social plans, or go to ER/urgent care, that is not normal.
Other common symptoms[1:41:14]
• Deep-penetration sex that hurts, chronic bloating (even outside periods), painful bowel movements, and recurrent bladder/UTI-like symptoms with negative cultures are red flags.
• Chronic pelvic pain that evolves from cyclical to constant is typical as disease progresses.
• She says women can largely self-diagnose based on these symptoms even without special tests.

Pathophysiology and progression of endometriosis

Retrograde menstruation and immune dysfunction hypotheses[1:47:12]
• A leading theory is retrograde menstruation: menstrual blood flows backward through the tubes into the pelvis, depositing endometrial cells.
• In most women, a healthy immune system clears those cells, but in susceptible women, immune dysfunction promotes their survival and implantation.
• She believes chronic inflammation seen in PCOS may be one reason PCOS patients frequently also develop endometriosis.
Local estrogen production and nerve growth[1:48:21]
• Implants initially depend on ovarian estrogen but then begin making their own estrogen locally.
• They recruit blood vessels and grow nerve fibers; each lesion can become highly innervated and exquisitely painful.
• Central sensitization of the nervous system amplifies pain signals over time.

Endometriosis and fertility

How endometriosis impairs conception[1:49:49]
• Pelvic inflammation can scar fallopian tubes, damage egg quality, and cause adhesions between bowel, bladder, and reproductive organs.
• Endometriomas ("chocolate cysts") inside ovaries can devastate egg count and quality, sometimes leaving a 30-year-old with zero eggs.
• The inflammatory environment can kill sperm, interfere with fertilization, cause ectopic pregnancy, or lead to early miscarriage.
• She states endometriosis is a leading cause of infertility and that average diagnosis age is about 32, long after years of pain and damage.

Diagnosis and treatment of endometriosis

Limitations of imaging and need for skilled laparoscopy

Ultrasound, MRI, and their blind spots[2:00:28]
• Pelvic ultrasound can detect endometriomas but usually misses superficial or deep endometriosis.
• Even pelvic MRI can be normal despite significant disease; normal imaging does not rule out endometriosis.
Laparoscopic resection as gold standard[2:02:30]
• Gold-standard diagnosis and treatment is laparoscopic surgery with excision (cutting out) of lesions rather than burning them.
• She notes that out of 100 gynecologists, only about one is truly trained to do proper laparoscopic endometriosis surgery.
• About half of surgeons given a laparoscope will miss stromal endometriosis lesions and incorrectly tell patients they don't have the disease.

Stromal endometriosis and subtle lesions

Difference between glandular and stromal lesions[2:03:55]
• Typical glandular lesions appear as black or purple blood-filled spots, easier to recognize.
• Stromal endometriosis lacks obvious glands and instead appears as thin fibrous lines that can be hard to see and are often missed.
• She says stromal lesions often produce more bloating, inflammation, and deeper pain and tend to respond less to progesterone alone.

Hormonal suppression strategies

Progesterone-based suppression[2:02:34]
• Most implants grow with estrogen and slow under progesterone, so first-line therapy is hormonal suppression with progesterone.
• She uses progesterone-only birth control pills or progesterone IUDs (e.g., Mirena, Kyleena) to suppress endometrial activity in many patients.
GnRH antagonists (e.g., Orilissa, Myfembree)[2:03:46]
• GnRH antagonists reduce estrogen production, creating a pseudo-menopausal state and significantly reducing pain, especially painful sex and periods.
• Side effects include hot flashes and other low-estrogen symptoms; because of bone loss risk, use is limited to about two years.
• For severe (stage 3-4) disease, she often combines surgical excision with progesterone IUD and sometimes adds GnRH antagonists for 6-24 months postoperatively.

Staging and pain-severity mismatch

Stage does not correlate with pain[2:04:30]
• Endometriosis is staged I-IV based on extent, but pain severity does not correlate with stage.
• A stage I patient can be in the ER monthly from pain, while a stage IV patient may have only mild discomfort.

Systemic problems in women's health care and advocacy

Dismissal of women's pain and mental health

Stories of extreme dismissal[1:30:06]
• She describes a 50-year-old patient who begged her not to call her crazy and had been told by prior doctors that her problem was "between her ears."
• Another patient in her 50s had visited roughly 100 emergency rooms and doctors over decades for pain, lost jobs, avoided relationships due to painful sex, and was never correctly diagnosed.
Comparison to male conditions[2:50:50]
• Aliabadi argues that if men had a condition causing severe pain during sex, scrotal scarring, lowered sperm counts, and frequent work absences, it would be treated as a national emergency.
• She notes that progress on Viagra and other male-focused treatments has historically moved much faster than women's health advances.

Structural problems in OB-GYN practice

Lack of pelvic ultrasound in routine care[25:22]
• Many gynecologists do not perform pelvic ultrasounds as part of a well-woman exam.
• Aliabadi considers ultrasound essential, comparing not doing it to taking away someone's glasses and asking them to read.
Separation of obstetrics and gynecology training[3:09:55]
• She proposes splitting OB and GYN into separate residencies so OB doctors focus on pregnancy and delivery and GYNs can focus intensively on complex women's health conditions.
• She recounts delivering 80-82 babies a month while pregnant herself and then seeing 30-40 GYN patients the next day, questioning how any doctor could do detailed diagnostic thinking under that load.

Redefining the well-woman exam

Current vs. ideal practice[3:15:40]
• She says a typical "well-woman" visit currently consists of a Pap smear, optional STD check, discussion of birth control, breast exam, and a mammogram order at 40.
• Her ideal exam includes fertility assessment, egg count, pelvic ultrasound (for fibroids, cysts, septum), screening for PCOS and endometriosis, lipid panel, APOB, lipoprotein(a), APOE4, bone health, colonoscopy timing, and genetic cancer testing where appropriate.

Fertility workup framework and autoimmune factors

Buckets of infertility causes

Female factor[2:34:05]
• Check hormones including AMH (egg count), thyroid, prolactin, and screen for PCOS and endometriosis.
Male factor[2:34:05]
• Order a semen analysis; consider history of radiation, testicular cancer, heavy cannabis use, or prior fertility issues.
Anatomical factors[2:34:22]
• Use ultrasound to look for fibroids, uterine septum, and cysts; evaluate tubal patency and pelvic adhesions.
Endometriosis and PCOS buckets[2:34:58]
• Actively assess for endometriosis using the symptom profile, regardless of imaging findings.
• Assess for PCOS with cycle history, androgen symptoms, ultrasound, and AMH; understand that many PCOS women don't ovulate even with regular cycles.
Autoimmune bucket[2:35:54]
• She highlights antiphospholipid syndrome and other autoimmune conditions that create hypercoagulability, causing placental clots and recurrent miscarriage.
• Endometriosis itself is framed as an autoimmune condition; she urges a full autoimmune panel in women with miscarriages, endometriosis, or family history of autoimmune disease.
• Treatments like low-molecular-weight heparin (e.g., Lovenox) in pregnancy can improve outcomes for certain autoimmune-clotting profiles.

Breast cancer lifetime risk and early screening

Calculating lifetime breast cancer risk

Average risk and high-risk thresholds[2:38:20]
• Average American woman has a 12.5% lifetime risk of breast cancer; about 12.5 out of 100 women in any room will develop it.
• Risk categories: low (<15%), intermediate (15-20%), and high (≥20%).
Tyrer-Cuzick (Tyrer-Cusick) risk tool[2:40:23]
• She emphasizes that every woman who knows her name and date of birth should also know her lifetime breast cancer risk via tools like Tyrer-Cuzick.
• Inputs include age, height, weight, breast density, reproductive history (age at first birth), family history, and genetic factors.
• Her site (SheMD) offers the Tyrer-Cuzick calculator free so women can know their personal risk.

Screening recommendations based on risk

Why "start mammograms at 40" is incomplete[2:41:30]
• The message that mammograms begin at 40 applies only to very low-risk women.
• Women with a lifetime risk ≥20% should begin breast imaging (e.g., mammogram and ultrasound) at age 30.
Role of MRI and genetic testing[2:43:09]
• High-risk women with dense breasts may need yearly MRI in addition to mammograms and ultrasound.
• Insurance is more likely to cover MRI if the doctor writes the calculated lifetime risk on the order (e.g., "lifetime risk 28%").
• She uses a company (Myriad) that both assesses genetic mutations (like BRCA) and refines risk by incorporating small genetic markers plus Tyrer-Cuzick results into a composite risk score.
• Women with very high risk (≥35%) can consider preventive strategies like intensive imaging, tamoxifen, or even prophylactic double mastectomy.

Her personal breast cancer story

Biopsy, risk calculation, and prophylactic mastectomy[2:45:32]
• At age 48, with no family history and no known genetic mutation, she had a breast biopsy showing atypia.
• Her Tyrer-Cuzick lifetime risk calculated to 37%; she likened boarding that risk to boarding a plane with a 37% chance of crashing and decided to remove both breasts.
• Multiple doctors resisted, labeled her paranoid, and one surgeon told her the day before surgery, "We have really good chemo for breast cancer."
• Final pathology after mastectomy found breast cancer in her right breast, confirming her decision and illustrating how risk tools can be life-saving.
• She notes that 85% of women who get breast cancer have no family history and fewer than 5% have known genetic mutations.

Perimenopause, menopause, PMDD, and postpartum depression

Perimenopause and menopause symptoms

Timing and symptom clusters[2:27:11]
• Average age of menopause is about 51.5; perimenopause typically spans 7-10 years prior (mid-40s but can start late 30s).
• Symptoms include hot flashes, night sweats, irregular periods, weight gain, painful sex, frozen shoulder, hair loss, and skin thinning, often with mood changes and sleep disturbance.
• She says many women with perimenopause are undiagnosed and not offered hormone replacement until after full menopause.
Endometriosis and menopause[2:53:18]
• Endometriosis pain generally improves after menopause because ovarian estrogen production declines.
• However, giving unopposed estrogen to women with past endometriosis can reactivate implants; she always includes progesterone in HRT for these patients, even after hysterectomy.

PMDD (premenstrual dysphoric disorder)

Definition and pattern[2:51:43]
• PMDD is a severe form of PMS where symptoms start ~10 days before menses and remit 2-3 days after onset of bleeding.
• Women may feel normal for two weeks and then experience severe depression, anxiety, crying spells, anhedonia, and functional impairment for the other two weeks.
• She notes high suicide risk during the symptomatic phase and says it stems from abnormal brain sensitivity to normal hormonal fluctuations.
Treatment approach for PMDD[2:53:23]
• She recommends SSRIs like Prozac (fluoxetine) 20 mg or Zoloft (sertraline) 25 mg taken only during the luteal phase (10-14 days before period) as very effective.
• She stresses evaluation for underlying generalized anxiety or depression and collaboration with psychiatry.
• In older women whose symptoms start new in their 40s, she considers perimenopause and may treat with hormone replacement.

Postpartum depression and its risk factors

Links to anxiety, PTSD, and PMDD[2:25:31]
• She says postpartum depression is more common in women with prior anxiety, PTSD, depression, or PMDD.
• She notes that PCOS and endometriosis patients often carry trauma and PTSD from years of dismissal and chronic pain, increasing their postpartum risk.
• The large hormonal drop after delivery can trigger severe mood changes, which families and providers may wrongly attribute to lack of sleep or stress alone.

Lessons Learned

Actionable insights and wisdom you can apply to your business, career, and personal life.

1

Women must be active advocates for their own health by learning key risk factors, symptom profiles, and tests, because many serious conditions like PCOS and endometriosis are frequently dismissed or missed in standard care.

Reflection Questions:

  • • What symptoms or concerns have I normalized or downplayed that might deserve a more thorough medical workup?
  • • How can I better prepare for my next medical appointment so I arrive with specific questions and requests (for example, AMH, pelvic ultrasound, or risk calculators)?
  • • Which trusted resources or experts could I use this week to educate myself about my own reproductive and hormonal health so I can advocate more effectively?
2

Treat root causes such as insulin resistance, chronic inflammation, and hormonal feedback disruptions rather than only masking symptoms with quick fixes like birth control.

Reflection Questions:

  • • Where in my own health or habits am I focusing on symptom relief instead of understanding and addressing underlying drivers?
  • • How could improving my sleep, movement, diet, and stress management realistically change my metabolic and hormonal status over the next 3-6 months?
  • • What one lab test or metric (for example, fasting glucose, A1C, or AMH) could I obtain this month to better understand an underlying pattern rather than just chasing symptoms?
3

Early measurement of egg reserve (AMH) and timely egg freezing can dramatically shift future fertility options, especially for women with PCOS or endometriosis, whose egg quality and quantity can decline much earlier than age-based charts suggest.

Reflection Questions:

  • • Given my age and family-building goals, when is the right time for me to measure my AMH and discuss my egg reserve with a knowledgeable clinician?
  • • How does knowing that age-based fertility curves don't apply equally to everyone change the way I think about the timing of children or egg freezing?
  • • What concrete step could I take in the next month (such as scheduling AMH testing or a fertility consult) to gain clarity about my current reproductive timeline?
4

Patterns of pain, bleeding, and mood across the menstrual cycle contain critical diagnostic information; tracking and respecting those patterns can uncover conditions like endometriosis and PMDD that profoundly impact quality of life.

Reflection Questions:

  • • What would I learn if I tracked my cycle, pain levels, mood, and energy daily for the next three months in a structured way?
  • • How might I communicate these patterns more clearly to a clinician so they see the full picture instead of isolated visits?
  • • If I notice recurring windows of severe pain or mood change, what specific questions will I ask my doctor about endometriosis, PMDD, or related conditions?
5

Risk calculators and structured frameworks (like breast cancer lifetime risk tools or infertility "buckets") can transform vague fears into concrete, actionable decisions about screening and prevention.

Reflection Questions:

  • • Which risk tools (for example, breast cancer risk calculators) are most relevant to my age, family history, and personal health profile?
  • • How could quantifying my risk change my willingness to pursue earlier screening, additional imaging, or preventive treatments?
  • • What is one risk assessment I could complete this month, and how will I use the results to have a more informed conversation with my healthcare provider?

Episode Summary - Notes by Jordan

Female Hormone Health, PCOS, Endometriosis, Fertility & Breast Cancer | Dr. Thaïs Aliabadi
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