I wonder who comes up with these strange, difficult to pronounce names for hormones, if etiocholanolone can be a hormone why can’t florpfloopistone be a hormone
That is funny
Whoa this thread goes fast.
Yes I’m seriously thinking that t4 only for Hashimotos is improper. I’d do Armor or t4+t3. No doubt about it. You’ll have to find a doctor that supports this way of thinking though.
Kinda unrelated but maybe take a look at high vitamin D supplementation (google Dr Coimbra’s protocols for immune diseases) and diets that keep blood sugar extremely stable (keto, or fruits only for carbs, the latter of which having my preference and is my way of eating)
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@tontongg great post. I like a little more carbs for hash, but agree blood sugar stability and armor are key.
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Hi @physioLojik, I wanted to ask you this in the thread dedicated to Dr. Crisler, but thought it would be too disrespectful there. You mentioned the cascade effects on downstream hormones just by manipulating a single hormone, like testosterone. Can TRT have negative effects on neurotransmitters in some individuals regardless of being on the “perfect” regimen for that individual?
To all of you guys who have emailed with specific questions etc - I will get to you guys as soon as possible! The response has been huge. Rest assured I’ll get to all of you ASAP!
I hope this is OK here as I’m partly asking Sir Mr Dr Sir, but I’m also happy to rely on others’ experiences too.
So, I started TRT a little over a year ago while training all along the way too. (It started out from rehab, turned into proper weight training.) Being 41 + being on TRT anyways + having lost quite much fitness and strength due to an accident and seven subsequent operations, almost losing a limb due to nosocomial infection, then having to learn to walk again after over a year in bed, all which happened a few years ago but most probably led to me needing TRT (head trauma, opiates, etc.) made me decide to give a blast a try. So this October I started a T-only blast. First 300 mg/w, gradually upping the dose to 500 mg/w. Luckily, i had almost no adverse effects. Obviously my lipids have taken a toll, but apart from that it’s only E2 that I learned I need to mind (and that too more mentally/psychologically than in ways of gyno, BP, etc.) I have an appreciable amount of belly fat (but nothing extreme, and decreasing), so no surprise.
After 16 weeks, I’ve now concluded the blast, and run labs.
T: 2,943 ng/dl
fT: 95 ng/dl
E2: 33.3 pg/ml → this was achieved by 0.5 mg of Arimidex/day.
My question is related to the clearance rate of T in lieu of further exogenous input, and especially in regards- and connection to E2 levels.
Accepting that everyone is different, but assuming that we can establish a rule of thumb, how long does it take for a free T of 95 to go down to ~25? During that period, how would you correspondingly taper down the AI?
Thanks for all the input in advance!
@so_it_goes What is your current test dosage? Did you do a taper or just decrease dosages after cycling
I took the last injection of 90 mg last Saturday, no Test since then.
The idea is to kind of wait until my levels drop to high-normal, and then maintain that. Two questions:
- how long should i wait for that, that is, when should I restart adding T to my body?
(on my own, I’d go for the usual two weeks ppl wait before their PCT [not a concern of mine], but …) - how to deal with AI until then?
(my guess is taper down)
I’ve started a trend! Yaaaaaaaaaayyyyyy
I like how you added the sir and the Mr before Dr before adding another sir into the mix, very classy 
Why do you take AI? The need for an AI is typically unnecessary and adds to long term risk to cardiovascular health, esp when cycling (look at literature, supraphysiologic doses of T or supraphysiologic doses of T + AI) When in conjunction with an AI HDL cholesterol tends to tank, without it, even on supra doses, the effect on the lipid profile (assuming the individual is only using testosterone) TENDS to be quite minor, however this is dependant on genetics, as some can take test only and have a trashed lipid profile while another might even take winny and have HDL/LDL in range (Unlikely though).
Estrogen is important for cholesterol metabolism and management, hence (one of the reasons) why non aromatising AAS tend to be so much harsher on the lipid profile.
Having optimal hepatic function will largely negate the need for an AI (liver regulates excess sex hormone exertion, shitty hepatic function can equate to too much E) try a more natural method, liver detox supps like NAC, Curcumin, Tudca (actually this is more of a pharmaceutical but yeet), cranberry, beet and carrot juice, lemon (I actually eat lemons by themselves lol #tootherosionrisk), etc etc.
Carrots are gross though, I don’t like them, unless they’re in matzo ball soup
Clinical trials (although small) haven’t shown a single healthy individual developing gynocomastia in the short term from doses 600mg or less
This is a theme. He has his own thread, received a lot of actionable advice, but just keeps asking. I think he wants a ‘diagnosis’ or label rather than a solution.
hey doc,
what is your opinion on staying on a supraphysiological test dose for extended periods of time (6-8 months)? I’m on TRT @160mg test-e/week, but for most of the year (6-8 months) I’m blasting at 500-600mg test-e, then I go back for a few months to 160. my bloods are all fine, I have no sides so far (been doing this for 2 years now). is this sustainable long term? what do I need to worry about?
last year I was at a cardiologist checking my left-heart wall (I dont know the english term) and it was 13mm, so slightly enlarged (10-12 is normal according to him, but 13 he said was absolutely fine and normal for TRT patients - he didn’t know about the blasting).
Also what do you think about mk677 if you are familiar with it? was thinking about stacking it to my blast @20mg every day.
Left ventricle. Many athletes have an increased thickness of the left ventricle (I’ve seen reports of supposedly NATURAL athletes (mostly ultra endurance and powerlifting athletes) having LVWT of up to 16-19mm, that being said the majority of individuals, even athletes will fall between the 10-12mm
The cause of athletic cardiomegaly is due to prolonged increase of cardiac output, thus the chambers of the left ventricle enlarge to compensate for frequently increased cardiac output. There’s two types of LVH, concentric and eccentric. I find the heart to be a fascinating organ, so if you wish for me to explain all this jazz in detail shoot me an email (in my bio) and I’ll be more than happy to talk about it.
Anabolic steroids tend to cause LVH through various mechanisms, and tend to exacerbate the LV hypertrophic response in response to intense weight training/ athletic activity. That being said, androgens appear to have a direct effect on the myocardium, cardiac myocytes contain androgen receptors, many actions of AAS are mediated by AR binding thus AR binding to cardiac myocytes = cardiac hypertrophy. The extent of the LVH will depend on lifestyle, genetics (someone with familial inhereted HCM will have a fucking huge heart on AAS lol, with equally huge arrythmogenic potential). Other mechanisms are, but not limited to, high blood pressure via excess sodium retention and other mechanisms caused by AAS, beta adrenergic receptor upregulation, oxidive stress and increased free radicals circulating in the body, (tachycardia induced cardiomyopathy for those extremely sensitive to this effect), individual amount of AR in cardiomyopathy and indirectly a shitty lifestyle, diet and whatnot will correlate with how big you’re heart gets on AAS.
Various supplements can help with oxidive stress and antioxidant dysfunction induced by AAS, I like Curcumin, coq-10, grape seed extract, garlic (I love garlic due to the taste lol), hawthorn berry and more, however just because you’re taking these supps doesn’t mean you’re risk free).
What’s the issue with an enlarged heart? If the left ventricular walls themselves become too thick, the amount of blood the heart can pump becomes impaired, or if it becomes too stretched (weak) the same occurs. LVH is arrythmogenic and increases you’re risk for deadly arrythmias like v-fib. What’s you’re resting HR? Most who have athletic cardiomyopathy will exhibit bradycardia. Do you have symptoms such as arrythmias, chest pain, synocope upon exercise, shortness of breath, swelling of the legs etc. The individuals (natural) I know who had HCM ( not family or related to me in any way ) only found out after they went into cardiac arrest, their ankles started swelling up etc. You need to get you’re cardiac function and output tested, a halter moniter might be good to see if you have any arrythmias throughout the day.
How many blasts have you run? What’s the highest dose you’ve used?
AAS aren’t harmless, it irritates me when people completely gloss over the potential cardiac risks. Be informed, stay smart, be safe.
Post could’ve been longer but I don’t want it being so ridiculously long you won’t read it lol
In my non professional opinion LV enlargement is only clinically significant if its associated with cardiac dysfunction. Other things that can cause LVH are (but not limited to) various cardiotoxic drugs (amphetamines, doxorubicin, cocaine), excess alcohol consumption, being a fat person, diabetes, being PREGNANT (although I don’t think you have to worry about that lol) and more
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I might have explained this earlier here, but maybe it was another thread. So, I used 300 then 400 then 500 mg Test (first blast, progressed with care), but subscribed to the philosophy you referred to and used almost no AI, partly also because my liver values were great. Then, I felt like crap, like real crap. I ran labs and found out that my E2 was over 80. Wow! So, I started the above Adex regimen, and guess what, in a couple days my brain fog lifted, my moodiness disappeared, I had will to live, and even had energy to play with our 10-month baby daughter and not just sleep all day.
My logic also involved the term you used “long-term”. That is, I was willing to trade short-term lipid compromise for actual functionality as a human being.
Makes sense?
Liver enzymes aren’t the only indicator of hepatic function, however I’m not going to go into that. If AI use works for you then go for it.
Did you get a complete liver Pannel done? What was you’re bf % and diet like (high in soy, processed foods etc?)
No soy, no processed foods (well, apart from the odd 5% treats maybe), but bf% not good. I have fat on my belly and trunk; funnily first striations show through on my delts now when I work out. Working on this. Actually, the plan now that I’ve got stronger and added some muscle (actually my arm grew 3 cm while my belly decreased 2 cm in 2018) to go back to the lowest possible TRT dose that keeps me going, hopefully without an AI, implement a light cutting diet (no extreme measures), maybe when my body (esp. lipids) has recovered from this blast, throw in some Primo in the spring to support this.
(and one more thing)
AI use working for me is one thing, but if smarter guys have a better solution option, I’d be a fool not to listen.
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Why is that? I’ve been running (I work out in the AM),
Pre-workout
50g oats
50g blueberries
20g whey
Intra-workout
50g waxy maize
10g EAA
Post-workout
100g oats
1 banana or some pineapple
250g low-fat cottage cheese or 2 scoops of whey.
Is this “bad”?
Doctor Mister Sir I have a question. Over the weekend when I had my shot due I accidentally took more than my TRT dose (had brought a prefilled primoteston syringe with the 19g needle but no syringe to backfill exact dose) I ended up taking around 230mg instead of my prescribed 200.
Over the past few days my libido has been insane (not going into deets but yea), I was wondering if the increase in libido was due to the higher test dose or a sudden change causing my body to be thrown out of homeostasis, and if this is the case, can’t I just slightly alter my test dose every couple weeks or so for a similar effect, like bump up a bit then go down.
I can’t believe a 30mg increase would make me THIS horny, it’s probably the sudden hormonal shift, however slight that throws my body slightly off track.
@unreal24278 it could be many factors - but in a trt thread I mentioned that I like to slightly alter my patient dosages so that they can bring themselves out of homeostasis every few weeks. Ie 120 a week to 140 a week to 120 a week and so on.