So not trying to start anymore drama with the round table or anything, but I just can’t stand to see these guys contradict themselves like this. They all say that water retention is not a side effect of high E2, and that it’s either in our heads, has more to do with our diet, or it’s from the testosterone, not estrogen. But at exactly 1:00:30 into the video, Dr. Rob Kominiarek reports that he has had guys come in on an ai, with very low E2, and in his words “they look great, the water’s all gone, they look like a million bucks”. While he’s saying this, Jay is nodding and agreeing. So my question is, if high E2 doesn’t cause water retention/ bloating, than why would someone lose a bunch of water weight and look so called “dry” when their E2 is lowered, due to using an ai?
TOT roundtable contradicting themselves once again
- Thread starter Gman86
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That’s a good idea. I’ll try to catch when they’re going live next Wednesday, and put my question in. Hopefully he doesn’t take it the wrong way. I’m always as respectful as I can be, so if he takes it the wrong way, that’s on him.
Will Brink
Member
Don't wanna sound all neg bag here, I'd add that I have known some guys to look great, only to fall over dead not long after. Low e2, made lower by an AI, is going to dump HDL levels, and whether it cosmetically makes them look leaner or not, men need E2, and I personally would not use how they look (unless they're competitive bbers only looking to hold that condition for a short time) as a metric of success in the big picture. Lowering E2 in an already lean man may have some added visual impact, but it's a bad idea and hard data is lacking as to what actual impact on bodycomp it has, be it BF or water or both.
PS, I will be on again Jan 31st.
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4PM
No doubt about it Will. E2 is extremely important for so many things, including cholesterol management, bone density, and overall cardiovascular protection, amongst many other benefits. You definitely can’t judge someone on how they look on the outside. I have a 40 year old male cousin that’s in good shape, and looks great, but has never worked out a day in his life, and eats insanely bad. Guarantee his insides don’t look even close to as good as he does on the outside.
Nelson Vergel
Founder, ExcelMale.com
LOL Everyone has an opinion. The fact is that most doctors do not take the time to review estradiol data. I have been obsessed with this topic for years and have read every single paper. But I have to say that we only know little of what the role of estradiol is in men. And nothing I can do or say will change the perception that estradiol is bad for men. Nothing.
Instead of wasting your time watching those TOT roundtables, take the time to read at least this paper. Most of you guys are smart enough to consume this information.
Chapter 24: Estrogens and Body Weight Regulation in Men
What would we do if we could not blame all evils (that have little data) of TRT on E2?!
Instead of wasting your time watching those TOT roundtables, take the time to read at least this paper. Most of you guys are smart enough to consume this information.
Chapter 24: Estrogens and Body Weight Regulation in Men
What would we do if we could not blame all evils (that have little data) of TRT on E2?!
You are wrong Nelson, you have absolutely changed the minds of thousands of men, in regards to estrogen, I guarantee it. I don’t think everyone is on board yet with 99% of guys not needing an ai, or having an E2 level in the 200’s or 300’s, or even 100’s, but you have absolutely made an impact. Pretty much nobody looks at estrogen anymore as an evil hormone that only benefits women, and I know for a fact that you had a HUGE role in that. It is sad that the TOT roundtable doctors basically came in and stole your thunder, and people really only started listening and accepting when they heard it from them, but you and Dr. Rouzier will always be the pioneers of this whole estrogen being beneficial movement, imo.
Nelson Vergel
Founder, ExcelMale.com
Thank you. Yes, Rouzier has definitely been upfront about the estradiol hysteria for years. Too bad he believes also that hematocrit should not be managed (I went to see one of his lectures at an aging conference in Florida)
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Ooo, already stirring up the pot on hematocrit huh Nelson? Lol. But ya I’m very much looking forward to his views on hematocrit, ever since he eluded to it at the end of the two part podcast he did with Jay. Well you never know Nelson, just like it took forever to convince all of us about estrogen, you might eventually be swayed in regards to hematocrit. Time will tell I guess. But again, very interested to hear his views. Hopefully the public gets to hear what he has to say on the matter soon. I’m sure it will be the new controversial topic soon enough.
Google "Dr. Rouzier hematocrit", then click on Videos.
Tednacious73
New Member
While I'm pretty new to TRT (about 2 months in), Nelson was the first person (on an old TOT roundtable) to alert me to the dangers of AIs. Then after reading more on this forum and watching watching many more roundtables I decided to stop my AI use. I always felt that Nelson has helped lead the way in a big part for the other doctors to have their current anti AI stance. Thanks Nelson!
He absolutely has. Took a little longer than he would of probably liked, but people are definitely coming around. I think there needs to be a tiny bit more open mindedness, and a little bit more emphasis on balance and respect for guys as individuals, but overall his hard work and dedication has definitely changed thousands of men’s views on E2, and for the better.
Nelson Vergel
Founder, ExcelMale.com
Thanks, guys.
Here is a recent great review on E2. I am trying to get the researcher to be on a webinar with me since she had led most of the recent studies:
Chapter 24: Estrogens and Body Weight Regulation in Men
Here is a recent great review on E2. I am trying to get the researcher to be on a webinar with me since she had led most of the recent studies:
Chapter 24: Estrogens and Body Weight Regulation in Men
This is a fascinating read, I am all in for that Webinar, I would love to see it.
Thanks
Is it not possible that when he says all the water is gone, he is referring to a situation where the person is extremely dry and not actually holding on to enough water? For instance, I'm pretty lean but I assume if I was taking a high dose AI that I would lose some water. That doesn't mean that I have water that I can afford to lose, just that it would be gone.
From watching the show, I get the impression that most of the doctors are of the mind set that reducing the dose would be best to reduce E2 symptoms. Dr. Nichols seems to always be an increase the dose guy and is pretty big on the creams instead of the injections. I for some reason was thinking that the cream would aromatize less which might account for his patients not needing an AI. Also thought that the cream would raise DHT which would help out with lidbo which I assume many patients are seeking TRT for.
DHT either suppresses E2, or suppresses the symptoms of high E2. Not 100% sure. I know it counteracts E2 in some way though. So there’s probably something to creams applied to the scrotum greatly increasing DHT, which then consequently allows the guy to have higher E2 while being asymptomatic.
Kind of guessing here, but presumably for the symptoms part DHT's higher binding affinity versus T and E2 helps bump out some E2. This also raises free E2 a little, causing faster excretion. A couple sites claim that DHT has AI activity, but I have yet to find a quality reference supporting the idea.
Nelson Vergel
Founder, ExcelMale.com
J Clin Endocrinol Metab. 1998 Aug;83(8):2749-57.
Comparative pharmacokinetics of three doses of percutaneous dihydrotestosterone gel in healthy elderly men--a clinical research center study.
Wang C1, Iranmanesh A, Berman N, McDonald V, Steiner B, Ziel F, Faulkner SM, Dudley RE, Veldhuis JD, Swerdloff RS.
Abstract
Twenty-five men, 60-80 yr old, participated in a pharmacokinetic study to compare three doses (16, 32, and 64 mg/day, n = 8 or 9 in each group) of 5alpha-dihydrotestosterone (DHT) gel (0.7% hydroalcoholic gel with 2.3 g gel delivering 16 mg DHT) applied daily over one upper arm (16 mg); both arms and shoulders (32 mg); and bilateral arms, shoulders, and upper abdomen (64 mg), respectively. Multiple blood samples for the pharmacokinetic profile for DHT and testosterone (T) were drawn over a 24-h period before application, after first application, and after 14 days of daily application of DHT gel. Additional blood samples for DHT, T, and estradiol were obtained 24 h after application on days 3, 5, 7, and 11 and after discontinuation of DHT gel for 3, 5, 7, and 14 days (days 17, 19, 21, and 28 after first instituting treatment). No skin irritation was observed in any of the subjects. Before treatment, mean serum DHT and T levels were not different among the three dose groups. The serum DHT levels increased gradually after gel application on the first day, reaching a plateau between 12-18 h. During the 14 days of daily application of DHT gel, the mean baseline DHT levels reached steady state by day 2 or 3 and were elevated considerably above baseline. Mean serum DHT levels varied between 8-11, 12-17, and 14-24 nmol/L in the 16-, 32-, and 64-mg groups, respectively. The area under curve (AUC) of serum DHT levels over 24 h on day 14 were 6.0-, 6.9-, and 16.1-fold above pretreatment levels for the three doses. Concomitant with the increase in serum DHT levels, the AUC produced by endogenous serum T levels decreased to 75, 56, and 36% of baseline after 14 days of 16, 32, and 64 mg/day DHT gel. Similar patterns of decreases in AUC of serum estradiol levels were found. The calculated mean total androgen levels (T + DHT) rose with DHT gel application in all groups (P < 0.0001) on both days 1 and 14. We conclude that the three doses of DHT gel tested might provide adequate androgen replacement in hypogonadal men at the low, middle, and high physiological androgen (T + DHT) range.
J Clin Invest. 1984 Dec;74(6):2272-8.
Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.
Casey RW, Wilson JD.
Abstract
Feminization in men occurs when the effective ratio of androgen to estrogen is lowered. Since sufficient estrogen is produced in normal men to induce breast enlargement in the absence of adequate amounts of circulating androgens, it has been generally assumed that androgens exert an antiestrogenic action to prevent feminization in normal men. We examined the mechanisms of this effect of androgens in the mouse breast. Administration of estradiol via silastic implants to castrated virgin CBA/J female mice results in a doubling in dry weight and DNA content of the breast. The effect of estradiol can be inhibited by implantation of 17 beta-hydroxy-5 alpha-androstan-3-one (dihydrotestosterone), whereas dihydrotestosterone alone had no effect on breast growth. Estradiol administration also enhances the level of progesterone receptor in mouse breast. Within 4 d of castration, the progesterone receptor virtually disappears and estradiol treatment causes a twofold increase above the level in intact animals. Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol from both control mice and mice with X-linked testicular feminization (tfm)/Y. Since tfm/Y mice lack a functional androgen receptor, we conclude that this antiestrogenic action of androgen is not mediated by the androgen receptor. Dihydrotestosterone competes with estradiol for binding to the cytosolic estrogen receptor of mouse breast, whereas 17 beta-hydroxy-5 beta-androstan-3-one (5 beta-dihydrotestosterone) neither competes for binding nor inhibits estradiol-mediated induction of the progesterone receptor. Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosterone-treated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor.
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