Sorry, will drop it I was just very impressed to see this thread.
No worries. Welcome to the forums, by the way!
I’d love to talk about the topic. But I have to keep correcting things attributed to me that I’m not saying.
Are you seriously this obtuse?
I understand the experience people have when they feel better when they use an AI, as opposed to when they don’t, BECAUSE THAT WAS MY EXPERIENCE!!!
They are feeling better on an AI, because their protocol sucks. They need to adjust either the amount of T they’re injecting, or the frequency of their injections, or possibly both.
Congratulations. You figured out all our problems.
Thank you Dr.
It’s actually pretty simple. There’s no reason to over complicate things. It’s not rocket surgery. And you don’t need to be a PhD to figure it out.
Are you a doctor being asked for your take on an official TRT protocol or something? Can you link me to this official guideline? Talk about obtuse. “I disagree with it so it is wrong”
Yes. About the reasons people get “banned” i dont think you need to look any certain way to discuss trt but your pompous ass attitude is unwarranted. You’re a fucking dickhead and hide on your circle jerk group where you think you have power. My anonymity is pointless. I can tell you who i am idgaf. Whats that going to do for you? Jack shit. You definitely wouldn’t pipe that cocky mouth off to my face thats for damn sure little man. And you “banned” me. Ta ta. Or whatever tf your gay ass comment was prior to doing so. Fact is when you have no comeback you ban. When you are at a loss of words or feel you are being genuinely challenged you ban. When one of your posse is made to look stupid you ban. Period. End of discussion. Have a nice life chump.
Although Danny is banned, I do and always have given him credit for raising awareness on these topics even if he always was reliant on his latest and greatest “smartest guy I know” to advise him how to analyze and take a position on complex topics. One legacy here of the “just keep increasing the T dose until your body finds balance” and “let E2 go where it wants to go” mantras will be it did provide a useful discussion construct to debate these ideas.
In this review paper, the problem (especially when confronted with EDCs, stress, lifestyle in today’s society) and potential solution is presented/thought of from a different angle. The idea of uncountered estrogen and more E2 is always better isn’t supported in scientific literature. Sure, uncontrolled AI use can pose risks but so can elevated intracellular E2 which can be damaging to male physiology. Would be fun to debate the merits of this paper and thinking especially in light of EDCs. Do you give the suffering patient more T or do you try to balance the low T / elevated E2 especially considering the possibility of upregulated aromatase?
For some years now, reduced testosterone levels have been related to obesity, insulin resistance, type 2 diabetes, heart disease, benign prostatic hypertrophy and even prostate cancer – often considered guilty more by association, than actual cause – with little attention paid to the important role of increased intracellular oestrogen, in the pathogenesis of these chronic diseases.
In the final stage of the steroidogenic cascade, testosterone is metabolised to oestradiol by P450 aromatase, in the cytoplasm of adipocytes, breast cells, endothelial cells and prostate cells, to increase intracellular oestradiol concentration at the expense of testosterone.
It follows therefore, that any compound that up-regulates aromatase, or any molecule that mimics oestrogen, will not only increase the activation of the mainly proliferative, classic ER-α, oestrogen receptors to induce adipogenesis and growth disorders in oestrogen-sensitive tissues, but also activate the recently identified transmembrane G protein-coupled oestrogen receptors (GPER), and deleteriously alter important intracellular signalling sequences, that promote mitogenic growth and endothelial damage.
This paper simplifies how stress, xeno-oestrogens, poor dietary choices and reactive toxins up-regulate aromatase to increase intracellular oestradiol production; how oestradiol in combination with leptin and insulin cause insulin resistance and leptin resistance through aberrant serine phosphorylation; how the increased oestradiol, insulin and leptin stimulate rapid, non-genomic G protein-coupled phosphorylation cascades, to increase fat deposition and create the vasoconstrictive, dyslipidemic features of metabolic syndrome; how aberrant GPER signalling induces benign prostatic hypertrophy; and how increased intracellular oestradiol stimulates mitogenic change and tumour-cell activators, to cause prostate cancer.
In essence, the up-regulation of aromatase produces increased intracellular oestradiol, increases ER-α activation and increases GPER activation, in combination with insulin, to cause aberrant downstream transduction signaling, and thus induce metabolic syndrome and mitogenic prostate growth.
To understand this fact, that raised intracellular oestradiol levels in men, induce and promote obesity, gynecomastia, metabolic syndrome, type two diabetes, benign prostatic hypertrophy and prostate cancer, rather than low testosterone, represents a shift in medical thinking, a new awareness, that will reduce the rising incidence of obesity, metabolic syndrome and prostate disease, and significantly improve the health of men worldwide.
► Do raised intracellular oestrogens in men contribute to adversely affect men’s health? ► Aromatase in oestrogen-sensitive tissues converts testosterone to oestradiol. ► Stress, poor dietary habits and xeno-oestrogens up-regulate aromatase. ► The resultant raised intracellular oestrogens activate proliferative ER-α and GPER’s. ► Aberrant signaling by oestrogens and insulin induce metabolic syndrome and prostate disease in men.
Oh yeah so high e2 is actually shit for you, such a damn surprise, no one could see that one coming … lmfao
That’s your response to these last two posts I put here? Hmmmm.
@readalot there’s some very technical reading in your last two posts and being slightly time crunched I dont really have time to read them.
Would you be so kind as to summarise a couple of the main and key points.
Since I’ve introduced a small amount of anastrozole I am
Happier (raised e2 was making me depressed)
Recovering from exercise better
WAAAAAAY less bloated (dropped 5kg water off in a short space if time).
One thing I keep coming back to is e2 causes prostate growth… 20 to 30 years with high e2 has got to be asking to be on alpha blockers when you’re in 60s and 70s?
Thats if I even get there- for all I know my TRT protocol is going to cut my life short.
Aromatase is a key enzyme in the transformation of androgen into estrogen. Its high expression will destroy the hormonal balance in the male body, and the excessive transformation of androgen into estrogen in the body will further damage the spermatogenic function of the testis, affect the normal development of the sperm, and cause spermatogenic disturbance. Adipose tissue has a high expression of aromatase and shows high enzymatic activity and ability to convert estrogen. Adipose tissue is the most estrogen-producing nongonadal tissue in the body because of its large size, accounting for about 20% of the body mass in healthy adults. PPAR γ is recognized as the key adipose differentiation in the transcriptional regulation of the transcription factor. In the process of adipocyte differentiation, PPAR γ regulate the expression of aromatase. The increase of aromatase is associated with the inflammatory response in adipose tissue caused by obesity. After obesity, the increase of proinflammatory factors in adipocytes will lead to enhanced transcription of the CYP19 gene encoding aromatase in adipocytes, which in turn will lead to increased expression of aromatase in adipocytes. This article reviews the regulation of male sterility from the angle of the “obesity-inflammation-aromatase” axis.
Glad you are feeling better and thanks for sharing. Just scan the abstract, figure captions or highlights bullet points if you are crunched on time.
Strange to me, this article seems a hot mess. I’ve yet to not drop bodyfat by thoughtfully setting up a 20% calorie deficit and switch to a low-carb, low insulin-secreting diet. I’ve scanned the range from 320 lb at +30% bodyfat to 200 lb at 6%BF and currently 235 lb at maybe 10% BF. Consensus I come to is to get your insulin levels down and if you measure fasting glucose please also add to that a fasting insulin. Big difference between pathologic insulin resistance in the morning (diabetes - high blood glucose + high insulin) vs physiologic insulin resistance (keto - highish blood glucose + low insulin).
I always feel night an day better once I control my E2 and bring it down. The problems I run into though is actually finding out how to make AI work long term. I almost have no choice but to cut my dose significantly as I can never find the sweet spot with AIs long term.
What is your protocol?
I’m only just dialling it in myself but having a fair bit of success.
Test I have 50mg eod (175mg per week).
Anastrozole 1/6mg eod (with the shot).
Seems to be working well- bloods in a week.
No, Im with you, sorry if i sounded condasending. I hate this anti-AI shit