Honestly it sounds like your gut is doing really well. The only way I can think to improve it would be to cut out dairy, gluten and limit sugar. And also get some good probiotics into your system on a regular basis. I personally use sauerkraut made from red cabbage. I get it from Whole Foods. This is obv assuming you’re not doing all these things already. But ya definitely let us know if you get accepted or not. Thanks.
low e2 symptoms didnt go away after crash
- Thread starter lowe2sucks
- Start date
Honestly it sounds like your gut is doing really well. The only way I can think to improve it would be to cut out dairy, gluten and limit sugar. And also get some good probiotics into your system on a regular basis. I personally use sauerkraut made from red cabbage. I get it from Whole Foods. This is obv assuming you’re not doing all these things already. But ya definitely let us know if you get accepted or not. Thanks.
My A1C is 4.9%, my sugar intake is fairly low. Dairy never bothered me throughout my 24 years of life so I am going to keep it for now since it's my primary source of calcium. I eat 2-4 greek yogurts a day so the probiotics are definitely there.
Has anyone experienced shortness of breath (or rather inability to take deep breaths at times), dizziness and chest pain while E2 either too low or too high? I have had echocardiogram, stress test and ECG, all have come clean (except for few skipped beats during recovery phase in stress test which has linked to increased heart disease risk but apparently because I didn't have any ST segment changes, I'm good?).
lowe2sucks
Member
it might be anxiety related. do you have any anxiety condition?
Yeah, definitely experience high levels of anxiety too. I had my e2 most likely crashed and feel like I experienced some type of rebound that made my e2 permanently higher. Just have been feeling this weird ache/pressure in my left shoulder and now lately some pain around my chest area. Trying to reassure that it could be just joint/bone pain in shoulder due to e2 deprivation, just weird that its only left one.
lowe2sucks
Member
it might be good idea to get it checked by the doctor to put mind at ease.. getting your e2 sensitive bloodtest done to confirm the e2 rebound wouldn't hurt too
Deleted member 16042
Member
Re cardiac, I've been there. My case may or may not be relevant to yours, but I used to have a couple decades worth of PTSD/anxiety provoked chest pain which turned out to be notably different from actual cardiac angina. Exertional angina prompted me to complain my way into getting a stress echo test which did turn up ST changes at about 12-13 minutes on the treadmill while I remained non symptomatic, and then lack of movement was observed in my left ventricle with echo. I was sent directly to the cath lab where angio showed I had 95-98% occlusion of my LAD for which I received a big ol stent.
With what happened to me, I would seriously avoid trying to talk myself into believing that what sounds like classic cardiac chest pain is attributable to high E2.
With what happened to me, I would seriously avoid trying to talk myself into believing that what sounds like classic cardiac chest pain is attributable to high E2.
Systemlord
Member
I'm on a E2 rebound after significantly lowering my AI dosage, I experienced the same thing yesterday driving to work for only minutes, it's the same ache under left armpit area, not where my heart is located. When E2 has been high for awhile this feeling under my left armpit area is constant, I wouldn't consider it pain though.
It's got to be some sort of hormone fluctuation or imbalance.
Thanks for the info, damn sounds like yours was a pretty close call. Only thing that is reassuring was that I did not experience any ST segment changes during the test, just few skipped beats during recovery. Felt pretty dizzy for awhile after it though.
Burritosnstuff
New Member
My left shoulder aches (joint pain). It ached worse and worse every time I took an AI and never gets better no matter how long I’m off AI. A Month ago I had bloods done and E2(S)was at 83 so I took 12.5mg aromasin, now it’s worse and even my right shoulder/collarbone hurts when I breath deep. Also when I wake up in mornings my feet ache. Literally hours after that aromasin I felt like the life was getting sucked out of me, fatigue, spacey, achy, upset stomach, anxious. Etc etc.
But I was having heart palpitations a lot when I was at my worst after initial crash. And my circulation has been horrible. My hands and feet start tingling at random times every day. Feet feel like they loosing circulation as it writing this. Maybe this has to do with the palps.
I stopped test cold turkey for 2 weeks and felt better for a few days, then like shit again days later, so I started Light test cream, didn’t notice anything, stopped then 2 days later felt good for another few days and now like shit again. Wtf...
Gonna stay off everything for a while and try a couple months of only HCG at 250iu EOD and see what happens, hopefully won’t push my E2 too high.
I feel like being off the test has been a step in the right direction because it had been 3 months straight with not one good day and now there’s are a couple good days here and there.
Idk much about this one, but Maybe what we are dealing with is progesterone imbalance???
WTFFFF is this???????
But I was having heart palpitations a lot when I was at my worst after initial crash. And my circulation has been horrible. My hands and feet start tingling at random times every day. Feet feel like they loosing circulation as it writing this. Maybe this has to do with the palps.
I stopped test cold turkey for 2 weeks and felt better for a few days, then like shit again days later, so I started Light test cream, didn’t notice anything, stopped then 2 days later felt good for another few days and now like shit again. Wtf...
Gonna stay off everything for a while and try a couple months of only HCG at 250iu EOD and see what happens, hopefully won’t push my E2 too high.
I feel like being off the test has been a step in the right direction because it had been 3 months straight with not one good day and now there’s are a couple good days here and there.
Idk much about this one, but Maybe what we are dealing with is progesterone imbalance???
WTFFFF is this???????
I seem to too have some circulation issues after this E2 disaster.
M
MarkM
Guest
Could it be that taking the aromasin is what is causing all your aches and pains? Aromasin is a suicide inhibitor and much stronger than anastrozole. Aromasin will prevent any estrogen rebound by permanently disabling the aromatase enzyme, while anastrozole cannot. So aromasin will basically wipe out all your estrogen and you won't have low E2 you will have no E2. You need estradiol for good bone health and when you completely knock it out you are going to have some of the symptoms you are describing.
Starting and stopping testosterone isn't helping how you feel either. While you might have low progesterone I think your problem comes from taking the aromasin to kill your estradiol verse trying to control it with a much more moderate AI like anastrozole.
A healthy male needs a certain amount of estradiol
Burritosnstuff
New Member
I would 100% agree with you, the problem is the initial issues came from arimadex. I only recently started messing with aromasin because arimadex messed me up so bad I was thinking maybe switching it up would help.
M
MarkM
Guest
I think you jumped into the frying pan when you went from arimidex to aromasin. That’s my best guess. Aromasin is so much stronger than Anastrazole/arimidex. Got to be real careful with that stuff.
madman
Super Moderator
Clinical Use of Aromatase Inhibitors in Males
AIs are classified as either type 1 (steroidal) or type 2 (nonsteroidal). Examples of steroidal AIs are testolactone, formestane, and exemestane, which inhibit aromatase activity by mimicking the substrate androstenedione. They irreversibly inhibit the aromatase enzyme by covalently binding to it; as such they are also known as “suicidal inhibitors.”
Nonsteroidal AIs inhibit enzyme activity by reversibly binding with the heme iron of the enzyme, resulting in competitive inhibition. Examples of nonsteroidal AIs are aminoglutethimide, fadrozole, anastrozol, letrozole, and vorozole (Table 1).
AIs are further classified into generations based on their efficacy. First generation inhibitors (e.g., aminoglutethimide) are relatively weak and nonspecific, whereas third generation AIs (e.g., letrozole and anastrozole) are most potent, most specific, and least toxic. Their pharmacokinetic properties (t1/2 of 48 hours for ansatrozole and letrozole and t1/2 of 27 hours for exemestane) allow for a once-daily dosing schedule. Their selective inhibitory properties negate the need for corticosteroidal or mineralocorticoid supplementation, which is essential for the nonspecific AI aminogluthimide. The second generation AIs are in between with regard to potency, specificity, and toxicity (e.g., formestane and fadrozole). Third generation AIs have been reported to have close to 100% inhibition of the enzyme, but this is not the case in males. In men, third-generation AIs will decrease the mean plasma estradiol/testosterone ratio by 77% [41,42]. This can be explained by the higher plasma concentration of testosterone in eugonal adult men compared with women. Because inhibition of aromatase is dose dependent, aromatase is less suppressed in the testis compared with adipose and muscle, thus explaining the incomplete efficacy of aromatase inhibition in males. The molar ratio of testosterone to AI and testicular aromatase activity is higher compared with adipose and muscle tissue. As mentioned earlier in this article, low estradiol levels are detrimental to bone health and sexual function. Thus, this incomplete suppression may be advantageous to men, and this lowers the risk of the potential side effects of AIs. Long-term use of potent AIs reduces circulating estradiol levels by 88% [43]. This is associated with adverse effects on bone [44,45] and could possibly be associated with increased body fat in men [22].
AIs are classified as either type 1 (steroidal) or type 2 (nonsteroidal). Examples of steroidal AIs are testolactone, formestane, and exemestane, which inhibit aromatase activity by mimicking the substrate androstenedione. They irreversibly inhibit the aromatase enzyme by covalently binding to it; as such they are also known as “suicidal inhibitors.”
Nonsteroidal AIs inhibit enzyme activity by reversibly binding with the heme iron of the enzyme, resulting in competitive inhibition. Examples of nonsteroidal AIs are aminoglutethimide, fadrozole, anastrozol, letrozole, and vorozole (Table 1).
AIs are further classified into generations based on their efficacy. First generation inhibitors (e.g., aminoglutethimide) are relatively weak and nonspecific, whereas third generation AIs (e.g., letrozole and anastrozole) are most potent, most specific, and least toxic. Their pharmacokinetic properties (t1/2 of 48 hours for ansatrozole and letrozole and t1/2 of 27 hours for exemestane) allow for a once-daily dosing schedule. Their selective inhibitory properties negate the need for corticosteroidal or mineralocorticoid supplementation, which is essential for the nonspecific AI aminogluthimide. The second generation AIs are in between with regard to potency, specificity, and toxicity (e.g., formestane and fadrozole). Third generation AIs have been reported to have close to 100% inhibition of the enzyme, but this is not the case in males. In men, third-generation AIs will decrease the mean plasma estradiol/testosterone ratio by 77% [41,42]. This can be explained by the higher plasma concentration of testosterone in eugonal adult men compared with women. Because inhibition of aromatase is dose dependent, aromatase is less suppressed in the testis compared with adipose and muscle, thus explaining the incomplete efficacy of aromatase inhibition in males. The molar ratio of testosterone to AI and testicular aromatase activity is higher compared with adipose and muscle tissue. As mentioned earlier in this article, low estradiol levels are detrimental to bone health and sexual function. Thus, this incomplete suppression may be advantageous to men, and this lowers the risk of the potential side effects of AIs. Long-term use of potent AIs reduces circulating estradiol levels by 88% [43]. This is associated with adverse effects on bone [44,45] and could possibly be associated with increased body fat in men [22].
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lowe2sucks
Member
i think you would feel better without any AI at all.. assuming you are not using very high dosage. i can see how one can feel bad when hes rapidly going from low e2 to high e2 but once you get used to high e2 you are gonna feel much better.
Hello I'm also in a similar situation dealing with long term sides after crashing E using aromasin for 3 months with no exogenous testosterone. I've learned a lot about be importants of estradiol. Here's a study I think that's interesting, shows androgen receptor bonding was increased 480% when estradiol was injected with a androgen. https://ntrs.nasa.gov/archive/nasa/casi.ntrs.nasa.gov/19850005159.pdf
Hello. Took some blood last week, been off everything of any dosage(serm, AI etc. for over a month) Bad symptoms persist. I feel EXTREMELY fatigued 24/7, my scalp is itching and I'm sweating a lot. Also get out of breath really easily now, I can barely walk, feel very weak. Stress test, ecg, echo was "normal" though so doctors are telling me it cant be my heart. Zero libido. My breast area randomly itches. But this bloodwork seems fine to me. Some problem with androgen/estrogen receptors instead of blood level? DHT has been at the very low end when tested.
Testosterone total: 23 nmol/l (10-38)
SHBG: 36 nmol/l (14-70)
Calculated free testosterone: 358 pmol/l (230-575)
Estradiol, sensitive: 25 pg/ml
Testosterone total: 23 nmol/l (10-38)
SHBG: 36 nmol/l (14-70)
Calculated free testosterone: 358 pmol/l (230-575)
Estradiol, sensitive: 25 pg/ml
Vince
Super Moderator
Your level don't look bad, could something else be causing your fatigue?
It does take time after crashing your estrogen levels feel right again, sometimes a few months.
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