Dr. Peter Attia
speaker
5,258 appearances
36 recordings
6 series
first heard Jan 2024
last heard Jun 2025
Dr. Peter Attia’s voice in public audio — every appearance, attributed to the second.
Trend
recordings per month · last 12 monthsNo recordings in the last 12 months.Older appearances are listed below; set an alert to hear about the next one.
Appearances
But you're going to start orally.
You're going to start at 100 milligrams, 50 milligrams.
Do we believe that 100 systemically is sufficient to oppose estrogen?
So the only thing that we do I would say different there is while we start women at 50 to 100, we will generally take them to 200 if tolerated, and if not, keep them where they are at 100. But we find women who are in that one-third to one-half group who are very positively selected towards progesterone, they feel fantastic at 200. The most notable improvement is sleep.
So would you agree with that? Totally agree. Most women are just over the moon with how well they sleep.
Hair gets thicker and mood improves. So now let's talk about the other subset of women. And this is a real subset.
It's, I would say in our population, it's about 10 to 20% for whom if you bring progesterone in the room, something goes wrong. their mood really changes. Now, it can in some cases become depressive, but more commonly what they tell me is, and I'm quoting them, this is not me saying it, I become a raging bitch. I'm worried I might kill my husband.
So for those women, we think progesterone's a bad idea. And we then use a progesterone-coated IUD. So are you doing that or are you using a suppository at that point?
Are you referring women who are on what potentially might be a low dose of progesterone to their GYN for endometrial ultrasounds on some regular interval just to look for hyperplasia or anything like that?
Okay. Anything else you want to say about progesterone? Do you start it concomitantly with the estrogen? Do you like to start one before the other?
I agree.
I'm really happy to hear. We're following your playbook already. So yes, we almost always start with estradiol and we muck around for a while till we get it right. That's why I saved it for last, by the way, because it's the hardest, in my opinion, in my experience to get right. Then we fiddle with progesterone and then testosterone if they're not already on it.
But to your point, some women are coming into perimenopause already on testosterone. Okay, let's talk about estradiol. There are two other estrogens. Estradiol is E2, but there's estrone, E1, and there's estriol, E3. Now the FDA only has a battery of approved products around the second estrogen, which is the dominant estrogen.
There's no FDA-approved product for estrone, and there's no FDA-approved product for estriol, but there are plenty of compounded opportunities around that. In fact, the most common of them is referred to as biest, biestrogen, which is an 80-20 mix of estriol and estradiol. What is your take on why that product exists? Do you view that as a reaction to the WHI? I mean, how do you think about it?
We don't use it at all. I have used it occasionally in the past, probably about 10 years ago, largely in women who were terrified of HRT. And to your point, it was viewed as, look, if you buy the argument, and this is a biochemical argument, there's no human data that demonstrate what I'm about to assert.
And again, I say this because one can look at a whole bunch of biochemical charts and tables and talk themselves into anything being true. But there are biochemical arguments to be made that estrone, and in particular one of the metabolites of estrone, and I think it's 4-hydroxyestrone, is the estrogen that is driving breast cancer.
So in an estrogen-sensitive breast cancer, given that you have so many estrogens, is it more likely that one is responsible than another? And so the answer is, oh, some of the data suggests it's 4-hydroxyestrone. Well, estriol has no biochemical path to even get there. In other words, there are no series of enzymes that can convert estriol into 4-hydroxyestrone.
And of course, there are pathways that will turn estriol weakly into estradiol. So maybe you get a little bit more. So there's a long-winded way of saying no reason at all from an evidence perspective to use it. We don't use it, have not used it in a decade, but that was my half-baked argument in certain situations. And in fact, I did use it once in a woman who had breast cancer.
was adamant that she needed hormones. Symptomatically, she really seemed to. Wanted it very badly. And I felt that this was a reasonable compromise. For what it's worth, she got insanely better on the biased. How much of that was from the estriol? How much of that was from the estradiol? I have no idea.
Yeah. And you mentioned this earlier. I think this is one of the biggest limitations of how I talk about this thing, medicine 2.0, which is very few people are conditioned to ask the question, what is the risk of not acting? We have a reasonable idea of what is the risk of doing X? What is the risk of doing Y? Although in this particular example, we seem to get that patently wrong.
Showing 481–500 of 5,258 · page 25 of 263
← Previous
Next →