HoldsUp

DavidPerlmutterMD · 2021-11-15 · Stephanie Estima, David Perlmutter (host)

Make Your Menstrual Cycle Your Superpower - with Dr. Estima | The Empowering Neurologist EP. 137

24 research-tied claims examined: 3 overstated 4 context 15 supported 2 unverified

4

Needs context

0:21:28Stephanie Estimaneeds contextmoderate

Plasma estradiol levels can increase approximately tenfold from early in the follicular phase to its apex just before ovulation.

"normally, in week one, towards the beginning of the week, if we were to look at some plasma estradiol, we might see, you know, levels of like five picograms per deciliter, seven picograms, like very, very low. And then towards the end of the week and then into the second week, your estrogen reaches apex. So it can go from—you know, I've seen labs where I've had women go from five picograms per deciliter all the way up to like 500, you know? So there's like a 10x, there can be a 10x change in a matter of days." (said at 0:21:28)

During a normal menstrual cycle, plasma 17β-estradiol concentrations rise substantially from the early follicular phase to a peak just prior to ovulation, often reaching a 5- to 10-fold increase (typically rising from baseline levels of approximately 20–50 pg/mL in the early follicular phase to preovulatory peak levels of 200–400+ pg/mL). However, the speaker misstated standard laboratory units (referencing picograms per deciliter instead of picograms per milliliter) and made an arithmetic error when describing a change from 5 to 500 as a tenfold (10x) increase rather than a hundredfold (100x) increase.

0:22:45Stephanie Estimaneeds contextmoderate

Unlike men who experience a 24-hour diurnal testosterone rhythm, women experience a peak in testosterone in the week just prior to ovulation.

"And so unlike men, who have more of a 24-hour rhythm of testosterone—they will sort of go through their testosterone and their estrogen cycle about every 24 hours—women will see that their testosterone will peak in this week just before ovulation." (said at 0:22:45)

While it is established that men have a prominent 24-hour diurnal rhythm in testosterone and women experience a statistically significant mid-cycle increase/peak in testosterone around the ovulatory window, the comparison requires important qualification. Women also exhibit a 24-hour diurnal rhythm in testosterone (with higher concentrations in the morning), and the periovulatory testosterone peak across the menstrual cycle is modest, highly variable between individuals, and often overshadowed by day-to-day fluctuations.

0:53:20Stephanie Estimaneeds contextlow

When equating for BMI, women require higher circulating leptin levels than men to experience satiety due to higher brain resistance to leptin signaling.

"Now for women, um for whatever reason, um we tend to, I mean, first we tend to have more adipose tissue than men, so there's there's that, but generally, um when we equate for BMI, so when we sort of, you know, pound for pound or BMI for BMI between men and women, women tend to need more leptin than our male counterparts in order to put the fork down, you know, to have that to have that feeling of satiety. And what that means is that we are generally more resistant, our brains are generally more resistant to the signaling, to the to the messaging that leptin is trying to tell us, which is put the fork down." (said at 0:53:20)

Women do exhibit higher circulating leptin levels than men at equivalent body mass index (BMI) levels, as confirmed by comparative human studies (PMID 15322603). However, attributing this sex difference to greater central leptin resistance or a higher threshold needed for the brain to experience satiety misrepresents the underlying physiology. Published evidence indicates that higher leptin levels in women for a given BMI are primarily driven by sex differences in body composition (a higher proportion of body fat and subcutaneous adipose tissue relative to men) and hormonal factors, rather than reduced brain sensitivity to leptin signaling.

0:56:46Stephanie Estimaneeds contexthigh

Reverse T3 is produced by the body and acts as a physiological brake when active T3 levels are elevated.

"reverse T3 almost acts as the brake. If there's too much active, if there's too much T3, your body will now start to produce more reverse T3. So it is like a mirrored form, if you will, um of of T3." (said at 0:56:46)

The speaker's description of reverse T3 (rT3) as a 'brake' and a structural isomer ('mirrored form') reflects the physiological role of the thyroid hormone inactivation pathway, but requires biochemical clarification. In humans, rT3 (3,3',5'-triiodothyronine) is produced from thyroxine (T4) via inner-ring deiodination by type 3 deiodinase (D3) and type 1 deiodinase (D1), rather than directly from active T3 (3,5,3'-triiodothyronine), which is instead degraded by D3 into 3,3'-diiodothyronine (T2). When thyroid hormone levels or signaling rise, the body upregulates D3 to inactivate circulating thyroid hormones, increasing rT3 production from T4 and reducing active T3 generation. However, rT3 itself is biologically inactive with negligible affinity for thyroid hormone receptors, serving as an inert clearance product rather than an active receptor-blocking hormone.

Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.