High estradiol number need advice

It depends a lot on hair loss. I’ve had no hair loss from Masteron, but I have had it from testosterone, for example.

If you care about hair loss, you should probably avoid most DHT androgens like Primo, Masteron, Proviron, or excessive testosterone dosages.

It also varies a lot sometimes in the past I had hair loss on 500 test, but on 1500 it wasn’t a problem. Even if you have no side effects from high estrogen, you should lower it. You can’t live like that long term at some point the side effects will occur, and along with high androgens, prostate problems are common.

What’s your height and weight? I’m 1.88 cm, 100 kg, and I get by with 175 mg testosterone undecanoate every week, one injection every Tuesday. That put me on 1100 testosterone and around 32 e2.

In my case, switching from test E to test U helped a lot with E2 and androgenic side effects.

But I still get a spike once every two months. I take 1/4 of a pill of Letrozole and that takes care of things, but it lowers it too much, so I’m probably switching to Arimidex. I just haven’t done it yet because it’s been working this way for years without problems I get semi-low libido for 3–4 days and that’s it.

If you have access to Arimidex do what I told you with 1/4th of a pill but with Arimidex instead of letrozole , but actually in your case letrozole would probably fit perfectly.

Im currently 5'9 about 205lbs. I would really like to get primo but its always fucking sold out on every sight!

Ive seen undecanote online but i dont think its available by script in Canada. Im on enanthate. I might get arimidex cause its cheaper
 
Im currently 5'9 about 205lbs. I would really like to get primo but its always fucking sold out on every sight!

Ive seen undecanote online but i dont think its available by script in Canada. Im on enanthate. I might get arimidex cause its cheaper
Primo is equally as bad in hair and for some dudes even worse but it has nice effect both on look and on controlling e2.
Undecanoate usually if you get it scripted it’s one big injection 5ml once every 12 weeks or so but u have to”tweaked” my regime and I do it every weed to keep things more stable an cause I’m a meat head lol.
I haven’t play too much with arimidex bu you would probably need more than 1/4th of a pill to get them sorted maybe 0.5mg , but I wouldn’t make a habit out of it not unless it’s scripted by a doctor AI’s usually lower the HDL.
 
Here's some more info on how estrogen plays a role in the human body and the effects that estrogen supplementation/replacement has on menopausal women as continued reading on the various ways it impacts the body

 
Estradiol itself has health benefits such as improving one's lipid profile (cholesterol)
...some ways to lower cholesterol?

Perhaps by improving it's rate of utilisation? If steroidogenesis slows down then naturally cholesterol will accumulate.

image.png


E is problematic which alludes to inadequate TRT management (quotes not my own):
Too much estrogen can also block the uptake of thyroid hormones, once again leading to symptoms of hypothyroidism.
Estrogen increases the synthesis of TBG, which binds thyroid hormone and decreases the amount of free thyroid hormone available to the body
Well, estrogen suppresses thyroid hormone and increases our need for TSH, while progesterone stimulates thyroid hormone.
 
Perhaps by improving it's rate of utilisation? If steroidogenesis slows down then naturally cholesterol will accumulate.

image.png


E is problematic which alludes to inadequate TRT management (quotes not my own):

The problem is that the graphic and quotes oversimplify physiology, reverse causality in places, and imply mechanisms more strongly than evidence supports.


A more accurate simplified model would be:
  • Thyroid hormone influences metabolic rate.
  • Mitochondria are required for steroid hormone synthesis.
  • Estrogen can increase TBG, especially oral estrogen.
  • Steroidogenesis uses cholesterol, but is not a major determinant of serum LDL in most people.
  • Endocrine systems interact, but not in the simplistic one-direction cascade shown in the image.
 
The problem is that the graphic and quotes oversimplify physiology, reverse causality in places, and imply mechanisms more strongly than evidence supports.

If one approach the graphic from a well-intentioned perspective that takes a rational outlook, then there are no interpretative issues.

A more accurate simplified model would be:
  • Thyroid hormone influences metabolic rate.
  • Mitochondria are required for steroid hormone synthesis.
  • Estrogen can increase TBG, especially oral estrogen.
  • Steroidogenesis uses cholesterol, but is not a major determinant of serum LDL in most people.
  • Endocrine systems interact, but not in the simplistic one-direction cascade shown in the image.

That's hardly simplified tbf. It's very convoluted. Can you explain your reasoning for why you wrote this?
 
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