Could Polyendocrine Metabolic Ovarian Syndrome (PMOS) be something you’ve been dealing with all your life? And if so, how would you know? And what would you do about it?
In a recent episode of Menopause Mastery, Dr. Betty Murray revisits PMOS, the condition formerly framed as PCOS, after her original episode struck a nerve with so many women. This time, she walks through her own personal history and breaks down the exact lab tests that reveal what most providers miss. We believe one in eight women is actually suffering with this condition, and the vast majority don’t even know it. If you exhibited some of the hallmarks of PMOS earlier in life but weren’t the classic “ovarian cysts, no periods, infertility” patient, you probably got missed.
Dr. Betty’s Story: The Early Signs at Puberty
Dr. Betty describes herself as petite and underweight until puberty, when “everything exploded in multiple directions.” Literally overnight, she went from being undersized and metabolically flexible to struggling with dramatic body changes and significant weight gain. Her periods were abnormal early on, though irregular cycles are also a common hallmark of starting puberty, which is exactly why these early PMOS symptoms so often get dismissed.
How Birth Control Hid the Symptoms
Like many women in college, Dr. Betty went on the pill. Birth control artificially suppresses natural ovulation, with synthetic hormones binding to receptors on the ovaries and blocking ovulation. The result? You don’t see the hallmarks of what’s really happening metabolically behind the scenes. But the metabolic activity is still there.
In a woman in her 20s or 30s with PMOS who is not on suppressive hormone therapy, labs would typically show elevated luteinizing hormone (LH), elevated androgens, and estrogen that is low relative to progesterone. Here’s what gets missed: you may still have normal periods without truly ovulating, and without developing ovarian cysts. If you’re on birth control, all of that is hidden while the metabolic derangement continues underneath.
Insulin Resistance Before Anyone Knew
Dr. Betty’s 20s and 30s felt like she had to do “heroic things” just to maintain her body weight. She was severely hypoglycemic, and a glucose insulin tolerance test in her mid-30s revealed the truth: her glucose didn’t rise radically, but her insulin was massively overshooting. Insulin’s job is to store fuel as fat, so she experienced hypoglycemic events, feeling shaky, sweaty, and lightheaded after any high-carbohydrate meal, even oatmeal with protein powder.
During her bodybuilding years, she lifted heavy six days a week and ate about 1,300 calories a day. She could get weight off, but it took two years of sheer willpower while feeling obsessed with food and starving the whole time. If that sounds familiar, insulin resistance in women may be the hidden driver.
Coming Off the Pill: Everything Changed
At about age 36, Dr. Betty came off the pill and got a tubal ligation. That’s when everything hit the fan. She started losing her hair, developed cystic acne across and under her chin, and packed on 35 pounds despite being a nutrition professional who knew exactly how to manipulate her diet.
Her cycles also began arriving closer together, about every 21 days. If your periods got shorter and closer together as you entered your 40s, that’s a luteal phase defect: progesterone isn’t climbing high enough, the follicular phase isn’t normal, and ovulation isn’t really occurring the way it’s supposed to. And here’s the trap: your day 21 estradiol and progesterone might look normal on a blood draw, so a standard perimenopause workup can miss the metabolic derangement entirely
Why She Was Told It Was “Estrogen Dominance”
The functional medicine community told Dr. Betty she was “estrogen dominant” and would gain weight because of it, which left her terrified of estrogen. Then came the testosterone pellet era. Her testosterone was low, her libido was gone, so she was put on pellet therapy. She felt great and regained libido, but gained another 8 pounds in three months.
Practitioners insisted it was water weight, claiming “testosterone causes weight loss.” That’s not true in women. Testosterone is an anabolic hormone, and when other androgens are high, it raises IGF-1, driving insulin resistance and fat storage through the IGF-1 and mTOR pathways, independent of insulin.
She later had an ablation for her “crime scene periods,” which removed even her ability to track her cycles. It wasn’t until she went back for her PhD that she pulled apart what was really happening: she was one of the PMOS women who was missed, because the old PCOS criteria required ovarian cysts and absent periods for a diagnosis.
PMOS Lab Testing: Where Most Providers Get It Wrong
Before we get into specific numbers, here’s the framework. PMOS lab testing is where most providers get it wrong, for three reasons:
- No single lab value tells the story. You have to read the patterns. Testosterone often looks normal, but is SHBG low? Free androgens are often elevated, but if you’re not looking at all the androgens, like androstenedione, androsterone, and DHT, you might miss it.
- Lab “normal” ranges are not optimal ranges. Insulin resistance starts well below the 24.99 flagged on labs. Anything over 10 signals major issues, and an optimal fasting insulin range is 2 to 7.
- Providers order the wrong tests. A perimenopausal workup usually covers FSH, estradiol, maybe testosterone, and a thyroid panel. What gets missed: fasting insulin, HOMA-IR, hemoglobin A1c, free testosterone, DHT, SHBG, DHEA sulfate, androstenedione, red blood cell magnesium, and inflammatory markers like hs-CRP.
The Lab Tests That Matter for PMOS
Fasting Insulin
This is probably the single most important test every woman needs, especially if you’ve “aged out” of an easy diagnosis because you’re no longer cycling normally. In early insulin resistance, the pancreas compensates by producing more and more insulin while glucose still looks normal. Optimal is 2 to 7 in a fasted state. Readings of 8 to 10 raise PMOS concern, and 10 or above means something is going on. Elevated insulin directly worsens PMOS by driving androgen production in the theca cells of the ovaries and the adrenal glands, and by suppressing SHBG in the liver.
A 2013 study in Human Reproduction confirmed that insulin resistance is present in 65 to 70 percent of women with PCOS/PMOS regardless of BMI. That includes the atypical thin PMOS phenotype without weight gain.
HOMA-IR
HOMA-IR (homeostatic model assessment of insulin resistance) is calculated as fasting glucose (mg/dL) times fasting insulin, divided by 405. You want it under 1.5. Insulin resistance is present above 2, and significant above 2.5. You can calculate your own using that formula.
Hemoglobin A1c
A1c reflects your average blood glucose over roughly 90 days. Standard normal is under 5.7, and a functional optimal is about 4.7 to 5.3. But it has limits: A1c can be falsely low in women with rapid red blood cell turnover, and it doesn’t catch early insulin resistance the way fasting insulin does. Use it alongside fasting insulin, not instead of it.
Fasting Lipid Panel and the Triglyceride-to-HDL Ratio
Doctors hyperfocus on cholesterol, but in PMOS the most important number may be triglycerides. When insulin resistance is high, the liver overproduces triglycerides, which also enables production of small dense LDL particles, the atherogenic kind that causes arterial plaque, even when your LDL looks unremarkable. Triglycerides should be under 100, ideally under 79. The triglyceride-to-HDL ratio should be under 2; above 3 is a significant sign of insulin resistance.
Fasting Glucose
Standard normal is under 100, but functional optimal is 70 to 85. Watch for a glucose that constantly hovers at 90 to 99 alongside a high fasting insulin. Your doctor may say “you’re cool,” but that pattern means insulin resistance is compensating and won’t stay that way. Women with PMOS carry a three to fivefold lifetime increased risk of developing type 2 diabetes, and 2023 research shows this risk accelerates during the perimenopausal transition. Many women get told they’re fine, then land on the menopausal side suddenly labeled pre-diabetic because it was brewing behind the scenes.
Total and Free Testosterone
Reference ranges vary wildly by lab, typically 15 to 70 in perimenopausal to menopausal women. Total testosterone misses the biologically active free fraction. A normal total testosterone can mask significant androgen excess if androstenedione, androsterone, or DHT are elevated. Clinically, women with total testosterone of 35 to 42 can still show significant hirsutism, chin hairs, scalp hair thinning, and androgen-driven acne when their SHBG is low.
SHBG: The Most Under-Ordered Test
Sex hormone binding globulin is produced by the liver and binds testosterone and estrogen, keeping them inactive. Insulin suppresses SHBG; estradiol stimulates it. Optimal is about 70 to 130. In PMOS, an SHBG under 40 significantly amplifies androgen activity even with low or normal testosterone. Insulin resistance, obesity, hypothyroidism, and oral estradiol drive it down. Transdermal estradiol, thyroid optimization, and improved insulin sensitivity bring it up. Many practitioners don’t understand this nuance.
Free Androgen Index (FAI)
Calculate it yourself: total testosterone divided by SHBG, times 100. Optimal FAI is under 4. In PMOS we often see 5 to 6 or above, accompanied by hair thinning, acne, and chin or mustache hair growth. Importantly, a 2020 study following women with PMOS through the menopause transition found that while total testosterone declined with age, the free androgen index remained significantly elevated compared to age-matched controls, particularly in women with insulin resistance. So in menopause you can look like everyone else on total testosterone while an elevated androgen index drives symptoms.
DHEA Sulfate
DHEA-S is the primary adrenal androgen, and adrenal androgen excess is commonly overlooked in PMOS. It tells you whether the androgen burden is primarily ovarian, adrenal, or both. Functional optimal is around 150 to 250 for women in their 40s. Elevated DHEA-S suggests adrenal androgen excess, often linked to HPA axis dysregulation and chronic stress. But note: low DHEA-S can occur later in perimenopause and is associated with fatigue, low libido, and mood instability. You can still have PMOS without an elevated DHEA-S.
DHT
Dihydrotestosterone is converted from testosterone by the enzyme 5-alpha reductase and is about seven times more potent than testosterone at the androgen receptor. Think hair follicles, fat cells, and acne. Most conventional labs don’t include it, so you must ask specifically. Elevated DHT with normal testosterone is common in PMOS. Even with normal blood DHT, receptor activity in the hair follicle can drive androgenic hair loss. Interventions include zinc, saw palmetto, and 5-alpha reductase inhibition with medications like spironolactone.
LH and FSH
In reproductive-age women with PMOS, the classic finding is LH elevated relative to FSH, usually around 2:1, because high LH drives ovarian androgen production. In perimenopause this gets complicated: FSH rises as ovarian reserve declines, which can normalize the ratio. Look for context. If FSH is climbing above 10 to 15, you’re in perimenopausal territory, but if LH remains disproportionately elevated relative to FSH, the ovarian androgen drive is still active.
Estradiol
Perimenopausal estradiol swings wildly, from 30 to 300, 400, even 500 and back. Watch the trend. A woman bottoming out at 20 to 30 is losing estradiol’s protective effect on insulin sensitivity and SHBG. If you’re still cycling, draw hormones on day 3 of your cycle to check the follicular phase baseline. If that’s off, it signals a follicular phase defect, likely paired with a luteal phase defect, even if your cycles seem normal.
Progesterone
Anovulatory cycles are a hallmark of PMOS, especially in perimenopause. You may have cycles without ovulating, and therefore without producing adequate luteal progesterone. On day 21 of a 28-day cycle (or 7 days post-ovulation), anything above 5 ng/mL indicates ovulation probably occurred, and above 10 suggests adequate luteal function. Low progesterone in the PMOS context contributes to sleep disruption, anxiety, and the “estrogen dominance” picture, because progesterone counterbalances estrogen and supports GABA. Key insight: if you’re a perimenopausal woman taking progesterone and your sleep, anxiety, and cycles aren’t improving, that’s a sign the underlying metabolic issue isn’t being addressed.
Full Thyroid Panel
You need TSH, free T3, free T4, reverse T3, thyroid peroxidase antibodies, and thyroglobulin antibodies. Ideal TSH is about 1 to 2, without suppressing it, since TSH and thyroglobulin independently support bone. The pattern that gets missed: free T3 can be low with a normal TSH because insulin resistance and inflammation impair T4-to-T3 conversion. Conventional endocrinology will tell you your thyroid is fine because TSH is normal, but a conversion problem still needs to be addressed. Elevated antibodies indicate Hashimoto’s, which commonly co-occurs and worsens through the menopause transition.
Hidden Markers Most Providers Don’t Check
hs-CRP (Inflammation)
Highly sensitive C-reactive protein is chronically elevated in women with PMOS. You want it under 0.5. In PMOS we typically see 1 to 3, and above 3 signals cardiovascular risk. A 2022 meta-analysis confirmed women with PMOS have significantly elevated inflammatory markers, including hs-CRP, interleukin-6, and TNF-alpha, independent of BMI. This is not a weight problem; it’s a biological phenotype. Test it with every blood draw (but not during acute illness or injury).
Vitamin D
Deficiency is nearly universal unless you supplement. Aim for 60 to 80. Vitamin D receptors are expressed on the ovaries and pancreatic beta cells, and deficiency worsens insulin resistance, impairs ovarian function, and amplifies inflammatory signaling. Multiple studies show that when women with PMOS start vitamin D, they see improved insulin sensitivity, reduced androgen levels, and improved menstrual regularity.
Red Blood Cell Magnesium
Target 5.5 to 6.5. Magnesium is a cofactor in over 300 chemical reactions, including every step of insulin signaling, glucose metabolism, and cortisol regulation. PMOS-associated insulin resistance drives urinary magnesium loss, creating a self-reinforcing depletion cycle, so most women with this condition need regular supplementation.
Beta-Glucuronidase (Stool)
This enzyme, produced by gut bacteria, removes the “wrapper” from estrogen compounds slated for elimination and pushes them back into the bloodstream. With gut dysbiosis, leaky gut, or a high animal protein diet, beta-glucuronidase rises, driving estrogen recirculation and worsening the estrogen-to-progesterone imbalance. Addressing it involves calcium D-glucarate, improving lactobacillus species, increasing dietary fiber, and supporting gut permeability.
The Three PMOS Patterns and How to Address Each One
Pattern 1: Insulin-Driven
The classic picture: fasting insulin 12 or above, HOMA-IR 2.5 to 3, fasting glucose in the 90s and above, triglycerides above 130, triglyceride-to-HDL ratio above 3, elevated androgens with low SHBG, elevated free androgen index, and elevated hs-CRP. Insulin resistance is the primary driver, directly suppressing SHBG and driving both adrenal and ovarian androgen production.
Start with insulin resistance first; everything else improves downstream. That means a high-fiber diet, insulin-sensitizing support like inositol, berberine, and alpha-lipoic acid, gentle time-restricted eating (stop eating about 3 hours before bed and fast 12 to 14 hours overnight), resistance training, more daily movement, at least one to two zone 2 cardio sessions weekly, and adequate vitamin D. Dietary change produces the fastest results here. Get the fiber up and insulin down before expecting weight change.
Pattern 2: Adrenal-Driven
Fasting insulin is borderline (7 to 10), DHEA sulfate is elevated or high-normal, total and free testosterone run high, DHT and androstenedione are likely elevated, cortisol is high with a morning spike and poor evening drop, hs-CRP is elevated, and free T3 is low despite a normal TSH. The HPA axis and stress system are the primary drivers, and cortisol is impairing thyroid conversion.
Women in this pattern present with anxiety, insomnia, hair thinning at the temples, and that classic “wired and tired” feeling. Start with HPA axis stability: sleep architecture, cortisol rhythm improvement, morning sun exposure and circadian support, adaptogens like ashwagandha, phosphatidylserine, and rhodiola, and magnesium glycinate with B6 at night. Address thyroid conversion with the right nutrients (zinc, appropriate iodine) or clinician-guided T3 support. Insulin work runs parallel, but the adrenal side must be dialed in first.
Pattern 3: Inflammatory-Driven
High hs-CRP, high fasting insulin, often elevated triglycerides, vitamin D under 25, low RBC magnesium, elevated beta-glucuronidase, and estrogen-recycling symptoms. This is where autoimmunity shows up: Hashimoto’s, celiac, and other autoimmune conditions. Symptoms include joint pain, bloating, and skin issues beyond acne, like rosacea, eczema, hives, and rashes, plus mood instability.
Start with the gut. Remove inflammatory dietary triggers, aggressively support vitamin D, omega-3s, and magnesium, feed the beneficial lactobacillus species, and get fiber in the diet. This is not the time for carnivore or hardcore keto; they make it worse. Calcium D-glucarate at 1,500 mg per day has been shown to reduce beta-glucuronidase activity and keep estrogen bound in the stool for elimination.
The Big Takeaway
PMOS is not a single disease, and it is not about cysts on the ovaries. It’s a syndrome with multiple phenotypes, insulin-driven, adrenal-driven, and inflammatory-driven, that often co-mingle. Identifying your primary driver requires a lab-guided, phenotype-based approach. This is why “exercise more, eat better, calories in, calories out” is wildly insufficient for women as a whole, and especially for a woman who may have been dealing with this her entire adult life.
Here’s your action plan:
- Pull out your labs. Look for the trends described above: fasting insulin, HOMA-IR, triglyceride-to-HDL ratio, SHBG, free androgen index, and hs-CRP.
- Listen to part one. Go back to the original June 24th episode on PMOS to understand why this condition is so prevalent and so often missed.
- Take the phenotype quiz. Visit quiz.gethormonesbalanced.com to identify whether you fit the insulin, adrenal, or inflammatory pattern.
- Find a PMOS-literate clinician. You need someone who can address hormones, adrenals, estrogen, testosterone, progesterone, DHEA, insulin, and thyroid together, and walk you through the dietary, lifestyle, and supplement changes you need.
- Build your team. Lasting results come from a triad of support, a nutritionist, health coach, and clinician, combining diet, lifestyle, exercise, stress management, sleep, and hormone balancing.
Dr. Betty lost the 35 pounds she gained as she worked through her own metabolic history using this exact framework. If your clinicians don’t understand this, consider it your wake-up call to find someone who does, because when you go into perimenopause and menopause, PMOS is still active, and without the right labs, you can’t see it.
Thank you for listening to Menopause Mastery. Watch the full episode on YouTube, and see you next week.