Dr. Natalie Crawford, MD, is a double board-certified OB-GYN and reproductive endocrinologist. We discuss how to improve hormone health at any age and the importance of fertility markers not just for pregnancy, but as a powerful window into overall health, vitality and longevity. We discuss hormone replacement therapy, egg freezing, IVF, and what biomarkers like AMH really indicate. Plus, how anti-inflammatory diets and specific supplements can be beneficial and the impact of microplastics and certain fragrances on hormones. We also discuss lesser-known factors that deplete male and female fertility, vitality and health. This conversation highlights how better understanding of hormones and your reproductive markers can empower better informed choices at every stage of life. Read the show notes at hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman David: https://davidprotein.com/huberman BetterHelp: https://betterhelp.com/huberman Eight Sleep: https://eightsleep.com/huberman Function: https://functionhealth.com/huberman
Crawford argues most women who might want kids should get an AMH blood test. She frames AMH as a rough measure of egg quantity, not egg quality, and says it can change life planning and earlier intervention choices.
Fertility is presented as a readout of hormonal, metabolic, and cellular health. Crawford notes infertility can correlate with higher risks of chronic disease because it can be an early warning sign of underlying issues like inflammation or insulin resistance.
Regular bleeding alone is less informative than knowing whether and when ovulation occurs. She explains that as long as cycles occur, they can reveal hormonal function, and perimenopause can include years of changing ovulation patterns while pregnancy remains possible.
Menopause is described as a single day defined retrospectively after 12 months without a period. Crawford argues this definition can delay help and that symptom-driven evaluation and earlier hormone support can be reasonable for some women.
Estrogen is often the first target when symptoms rise due to declining production, with progesterone added depending on ovulation and symptoms. Testosterone is discussed as a later and more individualized addition, given conversion pathways and variable need.
She links earlier ovarian failure with more ovarian fibrosis and inflammatory markers, and higher rates of autoimmune disease. The practical takeaway is that managing inflammatory conditions and lifestyle factors may help preserve ovarian function as much as possible.
Crawford expresses concern about microplastics accumulating in ovaries and endocrine disruptors correlating with worse fertility outcomes. She emphasizes reduction over perfection and treats toxins as one contributor to overall inflammatory burden.
She cites population data showing monthly conception probability declines with age but rarely reaches zero. She also notes some evidence that prior live birth with the same partner is associated with higher chances of conceiving again until the late 30s.
Even after a prior pregnancy, new barriers can emerge such as aging-related egg quality decline, sperm changes, or time-dependent conditions like endometriosis. She stresses earlier evaluation if attempts extend beyond expected windows, especially at older ages.
Crawford criticizes waiting 6 to 12 months of trying before basic testing like semen analysis, anatomy checks, and ovarian reserve. She argues earlier screening can prevent lost time in cases like blocked tubes, uterine anomalies, no sperm, or low reserve.
The discussion highlights that ejaculate does not guarantee sperm presence. Crawford notes clinics can perform semen analyses readily and mentions mail-in CLIA-certified options as a way to reduce gatekeeping and delays.
She validates the emotional burden of miscarriage while noting it confirms some reproductive functions occurred. She argues evaluation after two losses is appropriate and criticizes older norms requiring three losses before initiating a workup.
Egg quality is framed as genetic normalcy and cellular competence, especially mitochondrial function and chromosomal segregation. Ovarian reserve is treated separately as egg quantity, which can be approximated with AMH despite limitations.
She explains AMH varies and can be suppressed by prolonged non-ovulation states such as hormonal contraception or postpartum periods. Crawford disputes guidance to avoid AMH testing outside infertility, saying the information can still guide timelines and choices.
Crawford states AMH can be obtained out of pocket for about $79 in some settings. She argues withholding a relatively low-cost test is disproportionate given the downstream costs and time sensitivity of fertility decisions.
She recommends learning ovulation tracking rather than only cycle length tracking. Early ovulatory dysfunction can show up as luteal phase shortening even when cycles seem regular, which can prompt targeted evaluation.
Crawford describes a predictable pattern from luteal phase defect to delayed follicular response to irregular cycles and amenorrhea. She suggests this progression can be detected earlier when ovulation timing is monitored.
She debunks the belief that IVF or egg freezing “uses up” eggs from the vault. The medications stimulate the cohort already leaving the vault that month, reducing natural attrition rather than accelerating ovarian depletion.
Early IVF relied on timing a single egg and even abdominal retrievals, with low success. The ability to administer FSH to mature multiple follicles is described as a key advancement that transformed IVF and egg freezing outcomes.
Crawford supports broader coverage for fertility preservation but notes political and ethical opposition tied to embryo personhood and disposition. She emphasizes patient choice and tailoring approaches to beliefs, including limiting embryos created or fertilizing fewer eggs.
She says large studies show no higher long-term infertility rates after contraception overall. She distinguishes rapid return after combined pills, a short-term endometrial recovery window after progestin IUD removal, and potentially long delays after Depo-Provera.
Crawford states routine early termination is not linked to reduced future fertility in studies. She notes risk comes from complications like infection or heavy bleeding that can cause intrauterine scarring, often reflected by lighter periods afterward.
She warns that NSAIDs can prevent follicle rupture and therefore block egg release. She suggests limiting NSAIDs to the menstrual period for those trying to conceive, avoiding them around the fertile window.
Crawford emphasizes the months before conception as a high-leverage window for egg and sperm quality. She highlights sperm’s roughly 90-day cycle and argues the preconception period is when behavior changes can matter most.
She groups priorities into sleep, stress, muscle, food, and toxins. The idea is to lower chronic inflammatory burden and improve metabolic resilience rather than pursuing perfect avoidance of all exposures.
She links poor sleep with altered gonadotropin signaling and worse fertility metrics in both sexes. She recommends consistent sleep schedules, 7 to 9 hours, and notes luteal phase demands can increase sleep needs for many women.
Crawford notes low-dose melatonin may support fertility via antioxidant effects and physiologic timing, while warning against high-dose products. She suggests it may be more relevant for certain high-inflammation or IVF contexts than for everyone.
She discourages cold plunges during attempts to conceive due to concerns about blunting needed acute inflammatory processes. She also avoids recommending strong anti-inflammatory supplements like high-dose curcumin in routine preconception plans.
She describes NMN and related NAD-support supplements as promising mainly in specific subgroups like unexplained infertility where inflammation may be a driver. She contrasts this with supplements like CoQ10 that have more consistent human fertility data.
Crawford recommends a prenatal with folic acid plus CoQ10, omega-3s, and vitamin D as common preconception foundations. For male fertility support, she highlights L-carnitine and certain minerals like zinc and selenium.
High-dose biotin can distort lab assay readings for multiple hormones including estradiol, progesterone, hCG, TSH, and testosterone. She advises stopping high-biotin hair and nail supplements before hormone testing or IVF monitoring.
She calls cannabis one of the most concerning modifiable factors, citing associations with poorer sperm parameters, higher DNA fragmentation, higher miscarriage rates, fewer eggs retrieved, lower fertilization, and reduced live birth rates. She advises avoiding it when trying to conceive and during pregnancy.
Crawford says nicotine exposure is associated with worse reproductive signaling and that cigarette smoking clearly accelerates ovarian aging and earlier menopause. She suggests nicotine pouches are unlikely to be benign and notes strong negative effects on sperm.
She supports short-term cleaner eating to identify individual triggers and reduce inflammatory load. The fertility-oriented diet emphasized is high in fiber, whole foods, and healthy fats while limiting ultra-processed foods and excessive added sugars.
She notes studies linking higher plant-protein patterns to better ovulatory and fertility outcomes, likely via fiber-rich diets. She describes data associating higher red meat intake with poorer IVF embryo outcomes and higher endometriosis severity, while stressing nuance and food quality.
She emphasizes frequent exposures matter most and suggests choosing fragrance-free over unscented products due to masking chemicals. She also highlights thermal paper receipts as a notable BPA exposure source for high-contact workers.
Crawford is intrigued by low-dose GLP-1 use to reduce inflammation in suspected endometriosis or unexplained infertility cases. She distinguishes this from weight-loss use and stresses careful dosing to avoid excessive leanness that could impair reproductive signaling.
She describes add-on therapies used when outcomes fall short, including growth hormone during stimulation to improve egg maturity and embryo development in some cases. She discusses PRP with more promise for intrauterine use in implantation failure than ovarian PRP, which is more invasive and less settled.
She notes advanced paternal age can increase certain risks such as autism and de novo dominant mutations, especially after around age 50. She frames absolute risks as still generally low and emphasizes improving sperm health in the months before conception.