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Timestamps 00:00 Cold open: 200 years of menopause medicine 03:23 Welcome and roadmap 04:20 The HPG axis, follicles, and the FSH lag 09:11 STRAW+10 staging and the timing of perimenopause 13:47 Austin: the 49-year-old with a hormone panel 20:00 Loraine: the OB-GYN workup 28:00 Symptom attribution: what menopause actually causes 33:46 Austin: the all-estrogen patient 37:58 VMS duration and the KNDy mechanism (Avis, SKYLIGHT) 43:53 Austin: who actually gets fezolinetant 47:22 The WHI 24-year correction (Manson, Chlebowski, Boardman) 01:00:15 Modern prescribing today 01:06:52 Where the menopause-content space gets it right and wrong 01:11:50 Testosterone, compounded bioidenticals, and DUTCH panels 01:24:13 Takeaways What we cover The HPG axis and the estrogen shield: what is happening across the 35-year reproductive era and what changes at perimenopause

They can be naturally occurring or synthesized in the lab, making them incredibly versatile for applications in medicine, research, and industry

These peptides act on pathways that regulate insulin secretion, appetite, gastric emptying, and energy expenditure

Suppression of early oxidative stress In our study, early increases in SOD, CAT, and GSH levels, along with decreased MDA levels, indicate that anakinra can effectively control reperfusion-induced oxidative damage during the early phase

The brain is largely formed by PUFAs with high sensitivity to lipid peroxidation (Nunomura et al., 2006), motor neurons are highly sensitive to OS (Simpkins and Dykens, 2008) and the CNS has a poor antioxidant capacity with low activity of protective enzymes such as glutathione peroxidase (GPx), catalase (CAT) or superoxide dismutase (SOD) and poor capacity for cell regeneration (Fischer and Maier, 2015