Not aromasin either? Have you tried the hospital pharmacy? If there’s a fertility center or a foreigner hospital, they have things the local pharmacies don’t. I can get anatrozole, but there are only 3 pharmacies that stock it here, it took a little bit of looking to figure that out.
Arimistane, which is an unregulated supplement, will work in a pinch. It’s one of the few otc drugs out there that actually has some data backing up its claims.
Yeah tried all that and more. Thanks for helping though. Waiting for my fish oil and curcumin supplements to arrive now.
what you really need desperately is to lower BF%
Why the fuck are you just ordering more and more stuff to take at 30% BF? You are obese. That’s why your E2 is high. Given your diminished sexual function and obesity, your body likely has other serious issues. Stop taking drugs and supplements and whatever you can get your hands on and dial in your diet and get some exercise.
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Hey, guys, I need some advice again as I’m confused about what to do.
I’m on currently on my 6th week of test e at 500mg.
This is my second time and this time I decided to go without AI, I did listen to @physioLojik and @unreal24278 and some other respected vets.
It was all good until around week 5, when high estrogen symptoms showed, just like the last time:
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Moody most of the time, very mild depression.
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No desire to have sex, erections are fine and can finish without much problem, but I just don’t want to…
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Just in general not feeling great like you’re supposed to on Test, I feel much better natty.
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The only positive is size and strength gains.
So my question remains is no AI really a good approach? The whole T to E ratio? Cuz I don’t feel like I should. Or is estrogen at 20-30 really the best despite the supraphysiological levels of T??
Testosterone (total only, no option in my country to do free T test):
2566 ng/dl
Estrogen (E2):
105 pg/ml
Is that E2 or total estrogens?
Either way, I think 105 pmol/l converts to 28.33 pg/ml… Which I think is really low estrogen for a TT of 2566.
My TT right now at trough is 1192 and sensitive E2 is 41 pg/ml… This is on 140mg a week for TRT (40mg EOD)…and I feel great.
Are you taking anything to prevent aromatization of estrogen? I think you need higher estrogen, not lower… But everyone is different I guess.
I’m sorry that was a mistake, it is pg/ml and it is E2.
No I’m not, this time I’m trying to go without AI to see if I feel any better than last time as I’m not gyno prone.
Guys, please clarify one thing, physio and others say that Ai’s like arimidex reduce IGF-I levels but nolvadex is great…
But what about that it reduces IGF-I significantly? Increases SHBG levels? And somewhat affects GH?
Can somebody explain?
He’s stated several times that the decrease is not significant enough to make any difference.
Search IGF & physiolojik
Hello @unreal24278 since Physiolojik is mia, I have a couple questions in regards to TRT/Low dosage AAS usage & Anxiety.
I’ve suffered from severe anxiety and a very sensitive CNS ever since dabling with mdma 10 years ago.
The first post is centeral sensitivity disorder, second is visual snow, both were triggered for me by mdma, others have them randomly triggered throughout life, mine are forever. However the rarity of these diseases caused me anxiety, depression, dp/dr(Which are symptoms of these diseases).
I’ve been on ssri’s for 10 years, theres been new research coming out in regards to these diseases, one such that lowering my stress/anxiety keeps all my sensitivity at bay… the best I can describe how it gets is if you drink a bunch of preworkout and you’re overstimulated, thats how I get from stress/too much caffine/lack of sleep/anything over stimulating, except my vision gets staticy, my ears ring really hard, and even tactile sensations are strong, similar to what autistic children go through.
I began trt about 7 weeks ago, I find myself constantly ‘on edge’, very over stimulated, however still at bay. How does exogenous testosterone effect anxiety & neurotransmitters? Including GABA & glutamate.
I know that Test increases SERT, as seen in FTM’s. Which SERT is what SSRIs act upon, but according to studies anxiety and sensitivity also have a lot to do with GABA/Glutamate.
Another reason I’m asking you is you’ve posted similar symptoms I’ve had in the past (increased HRV, anxiety etc), My first injections my HRV went through the roof until I tweaked my protocol, I currently inject 25mg/ED w/ 5mg masteron
Have you evaluated your diet? Past antibiotic use? It is thought that we may produce as many neurotransmitters in the gut as in the brain, so your biome plays a part. Maybe some probiotics or even some yogurt would help. How is your gut health? And MDMA is a of course a great way to jack some things up. How do you react to 5-HTP?
I can’t take 5htp as I’ve been on an ssri for 10 years. My diet is great, I’m not overweight, its been 10 years, trust me I’ve tried a lot. As I said it’s a rare neurological condition. I honestly just need to know the effects of test/e2 on the cns/glutamate gaba as that seems to be the main perpetrator of my issue. If you’re curious you should youtube visual snow, pretty interesting condition and actually quite common, yet not understood which is why its rare.
It can’t be common AND rare, they are antonyms. I know that test is part of the dopamine cycle in your brain. You need free test to make dopamine, and serotonin and dopamine are somewhat mutually suppressive- meaning that if you do something to accelerate serotonin production you dampen dopamine production and vice-versa. Have you considered that maybe you don’t need the SSRI at all? Appropriate levels of free test can change your brain chemistry pretty substantially, and MDMA would have caused some serious dopamine issues, immediately followed by serious serotonin deficiency symptoms (receptor saturation).
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I understand/am aware of central sensitivity syndrome… I have fibromyalgia (though I don’t talk about it as I feel many don’t take it seriously due to lack of research/recognition of the condition… myself included). Fibromyalgia can be considered a variant of central sensitivity disorder, as amplification fo the CNS induces a heightened sense of pain at times (particularly burning, tingling pain etc) when there is no need for such sensations to be felt.
Can’t relate to the overstimulation however
So… Hallucinogen persisting perceptual disorder, that’s seriously unlucky… sorry mate, given we have very little research in the way of psychedelics due to the fact they’re (unfairly) schedule I (or equivalent) substances in most countries, thus the effects on neurology and how they effect people based on differing brain chemistry remains largely unknown, hence why some can take all the LSD, DMT, LSA, Psilocybin in the world and be fine while others will take one tab of LSD and go bat shit insane (uncommon, I don’t know of anyone to experience long term mental instability due to one bad trip, but I’ve seen literature reports), I do have one friend however who took LSD once and totally lost it (acutely), started breaking objects, forgot his name etc.
My issues are in relation to dysautonomia, both closely linked with benign joint hyper-mobility syndrome and fibromyalgia, there’s a strong correlation between all three conditions and thus a valid cause/effect relationship. High dosages (supraphysiologic) of certain compounds, particularly testosterone aggravate the condition due to increased sensitivity to catecholamine uptake at a receptor level. I have autism, however it’s high functioning in nature and appears to be beneficial in terms of overall intellect… but highly detrimental in the department of social skills and being prone to bullying, however having a decent amount of muscle mass has lessened people messing with me in person, and thus transferred to any bullying being words spoken about me behind my back, which I’m far more comfortable with (that or females pick on me instead because they know I can’t do anything to retaliate regardless of whether instigation is physical or emotional)
The mechanism as to how SSRI’s work remain confounding, we know they inhibit serotonin reuputake, hence the name selective serotonin reuputake inhibitor, yet we don’t know/have little knowledge in relation to many of the downstream effects these drugs have, nor do we fully understand the interactions these compounds have with other compounds (especially recreational drugs, serotonergic psychedelics antagonise the mechanism by which SSRI’s act upon 5HT receptors (certain subtypes yeet, I believe it’s primarily the 5HT2a receptor subtype but I don’t have the time to look into it as I’m right near exams)… but do they cause serotonin syndrome? Perhaps, perhaps not… why do some experience serotonin syndrome from SSRI use alone? We know SSRI use can induce pharmacodynamic drug interactions without change in the actual concentration of SSRI due to agonistic/antagonistic interactions with various drugs, yet which drugs/ how/why etc isn’t properly understood, all we know is that if two drugs target the same 5HT receptor, chances are there may be an interaction between the two.
As to glutamate, high doses of AAS may induce neurotoxicity via increased glutamate turnover (and various other mechanisms), this has been demonstrated within rodent models and implied within structural imaging of the brains regarding AAS users (heavy dosages). I believe in rodent models AAS alters glutamate receptor immunoreactivity at a receptor level, of which is correlated with aggressive behaviour. I can’t go through all the mechanisms here as it’d take way too long and I apologise but quite frankly I don’t have the time to explain. But AAS (differing AAS have differing neurological effects) may attenuate anxiety via interactions with neurosteroids, NDMA receptors, serotonin, dopamine, interference with GABAergic transmission, etc.
What I can say quickly as I’ve said many times prior, AAS up regulate sympathetic nervous system activity, both at rest and in response to exercise. Such up-regulation and increased sensitivity to catecholamine uptake (think beta adrenergic receptor upregulation etc) will fuck with you’re HR variability, both at rest and in response too exercise, some are far more sensitive to this than others (myself included given preexisting autonomic dysfunction), hence this resides in one of my hypothesis as to why some experience severe cardiac damage from AAS (AR induced cardiac myocyte stimulation for growth, lifestyle factors, catecholamic overload!!!)
Actually a recent study came out on the cardiac parameters of AAS user/controls (largest study too date) and the majority of the results weren’t particularly different from controls (appeared to be subclinical cardiac impairment) yet the box plot in relation to responses was extremely varied, and some subjects demonstrated substantial cardiac impairment, I’d hypothesise genetic variability/ sensitivity to such responses play a large role, as if you’re HR is resting at 90BPM+ and exertion brings it to like 180+ for prolonged periods of time (and HR recovery is impaired, leading to tachycardia for prolonged periods of time post exercise) this would equate to tachyarrythmia induced cardiomyopathy over the long term. My theory here is further supported by the fact that in many case reports, discontinuing use appears to largely reverse the cardiomyopathy. Granted there are many mechanisms behind cardiac damage here (high blood pressure, direct injury etc), however this is merely a THEORY I have…
Daily injections in my opinion are ridiculous, the hormonal fluctuation you’re experiencing from daily shots is minimal compared to e3.5 d, if it works for you then… great… but any benefit is likely placebo with long estered hormones, and furthermore SHBG has nothing to do with how a protocol should be created, it’s a transport protein that fluctuates wildly based on a myriad of variables… Unless you’re shooting test prop or TNE (or mast prop) I’d stipulate you’re probably wasting you’re time unless you’re some genetic anomaly that cleaves through hormones at accelerated rates (metabolises the ester → active hormone in rapid succession). If it works for you then, go for it… I’m not here to dispense dosage advice.
What’s the masteron for? I like it for libido/sense of wellbeing. Out of curiosity, has the experimentation with MDMA screwed up you’re response to all compounds (like can you smoke pot or drink a beer? I’d assume probably not)
I apologise if my message comes across as primitive in relation to grammar or knowledge dispensed, I’m short on time. Sorry to hear about you’re troubles however
I’m not Dr Sir, perhaps chuck him an email if you want medical advice on what to take. I can give recommendations but I don’t like doing so as I’m not qualified to write/prescribe protocols. Regardless of any base knowledge, I don’t have a degree, and that’s pretty much all that matters… I doubt he will respond though
I must say however I’m very happy the nickname Dr Sir took off, I find it hysterical… Only use formal prefixes to address physiologik, like Dr Mr Professor Sir Sire The second esquire… Make it as long and nonsensical as possible
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The crashes I see from people the days following high dose MDMA consumption look horrid
Hopefully that’s changing
In australia? With the liberals in power… not for another 100 years lol
Yes thats why I added masteron, also trying to troubleshoot my anxiety from by what I assumed was triggered by high e2.
Yeah I don’t have FM, but I can say all of my senses were intensified, like uncomfortable crawling out of my skin type intense.
Hppd/visual snow both share the same pathology, I’m sure my anxiety would have somehow triggered this eventually. I hate it, its changed/ruined my life, this started at 17, im 27 now, ive worked around it and do the best i can but stress intensifies it, so break ups and what not really make me look for answers.
Everytime I ever smoked weed (which was around 40 times) it was like a complete acid trip (over exageration)I’d get tunnel vision, ears would ring really loud, things I would touch fealt like they were cutting me, time slowed down, etc. Its weird because things like coke, adderall were totally fine… I’m fine with beer, it actually inhibits a lot of my senses and allows me to be my real self (which is why I don’t drink, i would get addicted). My research into phenibut/gabapentinoids actually lead me back into looking up hppd/visual snow as I havent paid attention to it, theres been a ton of research and big pushes made in the last 6 years. Lamotringe has helped in some cases, which seems to block glutamate and work on gaba a bit.
Funny about HRV, my resting HR is high 70s/low 80s, 90-100 bpm throughout most of the day. Working out I’m constantly at 180, this was pre trt and current trt. However after massive spikes it shot up resting to like 110
It was assumed rare, but as more awareness has been made its been found to be a little more common.
Ik I dont need the ssri and actually wanna get off which is why i started trt but this has sent me down anither rabbit hole.
Also ssri only.helps in the way of managing my stress anxiety, if that raises so do my symptoms of hppd