MESO-Rx
Anabolic Steroids
Low Estrogen
- Thread starter baja212
- Start date
the most obvious and troubling effect of long-term low (abnormal) E2 is osteoporosis. What are your E2 levels? And what meds/supplements are you taking?
hardasnails1973
New Member
joints hurt
emotional zombie
dick is dead
muscle flat
insulin issues
testosterone will not work for crap
fat bloated stomach
muscle atrophy
decreased memory.
increased altzihiemers probaabliity
emotional zombie
dick is dead
muscle flat
insulin issues
testosterone will not work for crap
fat bloated stomach
muscle atrophy
decreased memory.
increased altzihiemers probaabliity
OhNoYo
New Member
hardasnails, you state, "testosterone will not work for crap" when having low estrogen levels. Sir, this is very interesting, and I was wanting to know if you could possibly go more into that topic, if you don't mind?
My current level is <20 ng/ml. Is that even low? I was under the impression if taking exogenous test. your estrogen levels will rise. Presently, I'm taking Testim Gel. Does low estrogen bring on ED problems?
hardasnails1973
New Member
just enough estrodial sensitize testosterone receptors too much shuts it down..
To HAN and Dr Scally.
Do you guys think a TRT patient can keep e2 in health ranges with .25mgs 2 or 3 times a week, or what. Do you guys even think its necessary to control it on 150mgs test cyp/week? I was assuming yes...?
Whats too low? 15? Whats too high? Pm says 20 is perfect. Whats the thought. Can Adex be effectively used at doses below the manufacturers intended use?
Do you guys think a TRT patient can keep e2 in health ranges with .25mgs 2 or 3 times a week, or what. Do you guys even think its necessary to control it on 150mgs test cyp/week? I was assuming yes...?
Whats too low? 15? Whats too high? Pm says 20 is perfect. Whats the thought. Can Adex be effectively used at doses below the manufacturers intended use?
The story of estradiol effect in males is yet to be told except for the well-known and well-described effect in osteoporosis. There is no clear evidence that either low or high estradiol levels are causative to other conditions, including cardiovascular, neurological, and urological events. Any statements that high estradiol levels are responsible for erection dysfunction are unfounded. Even more ridiculous and bizarre is the contention that elevated estradiol levels somehow shutdown the androgen receptor.
Additionally, studies must consider that estradiol is synthesized from testosterone. Estrogens in men originate predominantly from peripheral aromatization of androgens and male adipocytes demonstrate a particularly high activity of aromatase, a key enzyme in estrogen synthesis. According to Arnlov et al, low estradiol concentrations have been related to increased risk for cardiovascular disease in white men from a community-based study in a Framingham cohort. In the literature, there is no consensus regarding the associations between circulating estrogens and cardiovascular risk in men.
Approximately 30% of men 60 yr old and older are estimated to have low testosterone, which is often accompanied by undesirable signs and symptoms such as low bone and muscle mass; increased fat mass (especially central adiposity); low energy; and impaired physical, sexual, and cognitive function.
Prospective cohort studies showing that men with low testosterone are at increased risk of falls; hip fracture (if estradiol is also low); anemia; type 2 diabetes; depressive illness; and, in some studies, Alzheimer’s disease. Testosterone insufficiency in older men is associated with increased risk of death over the following 20 yr, independent of multiple risk factors and several preexisting health conditions.
Estrogens have numerous biological effects in men and have a complex effect on the normal cardiovascular system. Many recent studies indicate that estrogens are as important as androgens in male physiology and pathophysiology, including their cardiovascular protective effects. Data regarding the role of estrogens in maintaining health in men comes from clinical and epidemiological studies in humans, animal experimental studies, and genetic diseases associated with estrogen deficiency in men (congenital aromatase deficiency and estrogen resistance due to specific receptor mutations).
Specific estrogen receptors are localized in the myocardium and vessel walls. There are links between certain polymorphisms of estrogen receptors (modifying tissue responsiveness to estrogen stimuli) in men and the severity of coronary artery disease, a risk of fatal and nonfatal myocardial infarction, and a risk of stroke.
Estrogens have beneficial effects on the myocardium and vasculature in men, such as attenuation of cardiovascular remodeling and reduction in cardiomyocyte apoptosis and necrosis. These cardioprotective and vasoprotective properties of estrogens may explain the link between low estradiol concentrations and an increased risk of cardiovascular events in a general male population. Recent experimental studies have postulated that the altered metabolism of estrogens and the deranged expression of their receptors may be involved in the pathophysiology of chronic heart failure (HF).
There is evidence that estrogen deficiency leads to disturbed glucose and lipid metabolism, and premature atherosclerosis in men. Physiological levels of estrogen have been reported to play a role in influencing plasma lipoprotein concentrations in men. When selective estrogen deficiency was induced in young men by administration of combined drug therapy with a GnRH antagonist (to suppress endogenous steroid hormones), testosterone (to restore testosterone levels to baseline), and testolactone (an aromatase inhibitor that prevents conversion of testosterone to estrogens), plasma high density lipoprotein (HDL) and apolipoprotein A-1 decreased, while plasma low density lipoprotein (LDL) and triglyceride levels did not change.
In a cross-sectional study, the relationships of plasma sex hormones to lipid and glucose metabolism in 212 apparently healthy men ranging in age from 18 to 59 yr. showed that the estradiol level was negatively related to both LDL cholesterol and fasting blood glucose, suggesting that the levels of estradiol within the physiological range for healthy men may help maintain a desirable profile of lipid and glucose metabolism.
Recent evidence from a 28-yr-old man with estrogen insensitivity caused by a disruptive mutation in the estrogen receptor (ER) gene suggests that estrogen may play an important role not only in bone metabolism but also in cardiovascular function. This individual presented with tall stature, normal masculinization, incomplete epiphyseal closure, and decreased bone mineral density. His serum estradiol and estrone, FSH, and LH concentrations were elevated, while testosterone was normal. Electron beam computed tomography scanning of the heart in this individual showed calcium deposition in his left anterior descending coronary artery, indicating early atherosclerosis. Lipoprotein analysis showed relatively low levels of HDL, but total and LDL cholesterol concentrations were also low, as were apolipoprotein A-1 and lipoprotein(a), while triglyceride concentrations were normal. Overall, these observations suggest that some actions of estrogen likely to be protective against the development of premature vascular disease in men.
Further evidence for a role for endogenously produced estrogen in normal male cardiovascular health comes from a condition in which a deficiency occurs in the enzyme responsible for the conversion (aromatization) of C19 androgenic steroids to the corresponding estrogens, involving the conversion of the delta 4–3-1 A-ring of the androgens to the corresponding phenolic A-ring characteristic of estrogens. Recently, a number of mutations of the aromatase gene have been described that give rise to complete estrogen deficiency. In men the most striking feature is continued linear bone growth beyond the time of puberty, delayed bone age, and failure of epiphyseal closure, thus indicating an important role of estrogens in bone metabolism in men. Such patients also have low HDL and increased total and LDL cholesterol concentrations and triglycerides, and hyperinsulinemia. Thus, it is possible that part of a putative protective role for endogenous estrogens in men is by maintenance of normal HDL concentrations and possibly by reducing LDL cholesterol.
To HAN and Dr Scally.
Do you guys think a TRT patient can keep e2 in health ranges with .25mgs 2 or 3 times a week, or what. Do you guys even think its necessary to control it on 150mgs test cyp/week? I was assuming yes...?
For the greater number of TRT patients, there is NO need for hCG or AI. I challenge anyone to find peer-reviewed literature in support of the use of an AI or hCG as a necessary need in TRT. I agree that in select patients this might be used, but this is very far from the norm.
First, i dont wnat to pick you apart and reveal all your trade secrets. So if it ever gets too much to answer, i understand.
My question is what E2 level do you see in the average 35 year old male on TRT with no other issues and body fat levels around 20%?
Further, Whats healthy? 20 -25? Do you think it is healthy for a persons E2 to rise proportionately with TRT or AAS. If TRT of 200mgs/wk were to drive E2 to say, 40, do you think this should be acceptable since it is a good number considering a "normal" corrolation to that dose.?
Sorry so busy today
My question is what E2 level do you see in the average 35 year old male on TRT with no other issues and body fat levels around 20%?
Further, Whats healthy? 20 -25? Do you think it is healthy for a persons E2 to rise proportionately with TRT or AAS. If TRT of 200mgs/wk were to drive E2 to say, 40, do you think this should be acceptable since it is a good number considering a "normal" corrolation to that dose.?
Sorry so busy today
Dr. Scally,
Any thoughts on ratio of T:E2 in a healthy male either on or off TRT?
I believe Dr. M. at one point said it was around 20-30.
My impression is that many guys are using AIs to drive their ratio way out of bounds. I personally felt best when my E2 was around 25 and my T was 800. However, I've struggled to keep my E2 that high for some reason.
Any thoughts on ratio of T:E2 in a healthy male either on or off TRT?
I believe Dr. M. at one point said it was around 20-30.
My impression is that many guys are using AIs to drive their ratio way out of bounds. I personally felt best when my E2 was around 25 and my T was 800. However, I've struggled to keep my E2 that high for some reason.
Yes, I was thinking that it would be nice to see the blood work of healthy 17 year old males for comparison and goals ( maybe not completely accurate reproduction
) I have already been there.
) I have already been there.
OhNoYo
New Member
Dr. Scally, from literature I have read and reviewed, I could not agree more. Estrogen in males is an extremely positive hormone to have in the body. Long-term estrogen suppression from AI can quickly bring down HDL levels so dangerously low levels, sometimes even in the single digits. In my opinion, both AI and SERMs are overused as well as used in excessive dosages. However, while I do feel that estrogen is great for a male in the correct amount, excessive estrogen can have dangerous side-effects, sometimes fatal, due to its pro-thrombotic conditions. Since it is now currently acknowledged that vulnerable plaque rupture is the leading cause of both fatal and non-fatal myocardial infarctions (MI), in theory vulnerable plaque rupture corresponding with high estrogen levels would augment any type of blood clot formation and significantly raise the risk of MI, wouldn't you agree (unless they were taking aspirin, Warfarin, or Plaxiv of course)? So, too low estrogen bad, right amount great, too much bad... 2 bad its just so hard to find an individual's sweet spot as different levels may produce positive effects in one person, but may cause negative attributes in another individual, correct?
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