For All You AI Preachers

Is this sarcasm? I can’t tell.

If it’s a legitimate compliment then thank you.

Big variables you guys aren’t even thinking of are lifestyle (ie smoking work alcohol environment stress) and diet. These are CRUCIAL components to observe mortality snd overall health. The biggest cause of any negative condition is inflammation - and this is related to the above variables much more so than test/ estrogen - at any level. @roscoe88 @unreal24278. I have seen patients with almost identical protocols Abdul hormone status levels yet one might be extremely high in CrP or have massively skewed ratios of EFA for instance from diet and stress. That guy is dramatically more likely to suffer a MI. Interestingly enough it’s these items (stress sleep life etc) that cause out of whack ratios to begin with.

3 Likes

These all impact hormonal parameters, I was referring to when an individual is symptomatic of high estrogen, however you’re totally right about lifestyles influence on these symptoms/ hormonal parameters. As to smoking, I’m not sure if you’re talking about tobacco or marijuana, however marijuana appears to have an estrogenic effect, hence the strong correlation between heavy marijuana use and gynocomastia, alcohol with a lot of hops in it has the same effect. I’ve never understood the allure of cigarettes, ALL my friends smoke them, I took one puff out of a cigarette when I was fourteen and was like “nope, never again”

As to inflammation are you talking about release of proinflammatory cytokines or generalised inflammatory markers.

@unreal24278 both. I don’t understand why people read studies and don’t realize that the samples don’t account for anything other than hormone levels. I’ve seen drastically obese people with “normal” sex hormone levels but they’re for sure going to drop dead in 5 years or less. Real world experience trumps studies over and over. If I take two people same age same sex same protocol same everything (including roughly same blood results) except for diet, stress, sleep, etc we can figure out which one will have negative outcomes over the long run. Studies never reveal this information so by and large a lot of studies are flawed from the beginning.

2 Likes

I’ve noticed this among many studies regarding anabolic steroids, the doses and health status of the individuals are always taken into question, however upon digging deeper into most studies you find the MAJORITY of the people in the sample are on hard drugs like cocaine, methamphetamine, opiates etc. One study was clever enough to weed out the drug users from just the AAS users, cardiac abnormalities were found (LVH, slightly reduced LVEF etc, nothing unexpected)

To add to this, I believe rat, mice and other rodent studies are a waste of time, frequently the results differ between how a mouse reacts and how a human reacts to a drug, we have different enzymes, pathways etc. In rats Dihydrotestosterone is a potent anabolic… In humans DHT is broken down by 3b-HSD and is therefore almost useless for getting hyooge.

Nope

@physioLojik:

Of your clients, are you privy to their death certs?

How many of your clients die of heart issues, of which there are plenty ?

I’m not disputing really anything you say except that unless you are personally comparing death certs and causes of death to one’s usage of trt then it’s hard to draw any conclusions.

Anabolic steroid use has been linked to heart problems for a long long time. Is it the test, or it’s metabloties, mainly dhea it e2?

Anabolic steroids effect the myocardium in a variety of ways, uncontrolled HBP→LVH, beta adrenergic receptor upregulation (esp by stronger androgens like tren) → potential prolonged sinus tachycardia → heart enlargement, androgen receptor minding to cardiac myocytes → cardiac hypertrophy, altered lipid profiles → atherosclerosis → myocardial infarction and more. Many of these can be mitigated with healthy lifestyle choices and careful planning, however the AR binding to cardiac myocytes is a problem, and what dose/duration causes serious issues is unknown. Hence why it’s best to get the most out of low doses, the guys who used lower doses back in the day (Frank Zane etc) are still alive today (well most of em) and I personally believe it’s due to the healthier lifestyles and lower doses employed that these guys aren’t dropping dead like flies.

That’s what’s interesting about SARMS. In a perfect world a sarm will exist that binds SELECTIVELY and solely to skeletal muscle tissue. Sparing the heart of serious enlargement.

Now intense weight training also causes LVH/CH, AAS allow you to train with ridiculous intensity, hence training induced LVH will also be magnified

This I believe.

I bet you the people who are on trt take care of themselves better. Track labs. Eat better and are more active. Is it the trt or the lifestyle trt gives you??

Rhetorical.

@charlie12 sadly no. Most people who seek out medical interventions want quick fixes and then are surprised when they actually have to clean up their act. Some patients get pissed that I require food logs.

3 Likes

Hmmm… It’s funny how we all read things differently. I interpreted what he said as meaning… if you/ we (the human race) would have been doing things right in the first place, you wouldn’t need the trt.

1 Like

My comment was related to how the studies can be unreliable as physio said. Studies mostly do not account for lifestyle, diet, supps taken, etc.

But i understand what I said about assuming someone on trt takes care of himself may be wrong. Physio would know better. I Take care of myself and assumed others would to on trt.

I can certainly see men inject testosterone and think"that’s it am good " and eat like shit

2 Likes

I understand. I am about 5 mins away from an anxiety attack and I am probably being argumentative.
I shall be be quiet now! :grimacing:

Yo what’s wrong? Why the anxiety attack

Was about to go to sleep but then saw this and now I’m not going to sleep @ChickenLittle

I should say I think i’d’ve been on TRT with or without a shitty lifestyle because my lifestyle when I was hypogonadal (aside from a lack of exercise) wasn’t that bad, plenty of sleep, relatively low stress aside from chronic pain, mediocre (but not as bad as a typical western diet) eating habits.

1 Like

I would be one of your greatest patients. I offer all sorts of data to my docs and they always scoff at it all.

@NH_Watts email me haha

1 Like

It’s just raining shit right now. It will pass. I’m going to go pick up heavy shit and hope for the best!

1 Like

Sent

I would like to share my experience here, as I asked for help on this forum in the past and got some help.
First of all, consider that for most us Europeans a sensitive estradiol test is a luxury, so I will be talking about regular E2 tests.
Long story short, I’ve been on steroids in my early 20s for 2 years, started taking Finasteride for massive hair loss and I’ve been on it for 7 years, even after dropping all the steroids, until my health was deteriorating so much I couldn’t just look away anymore. Once I realized Finasteride was the cause and being diagnosed as a PFS sufferer, I tried all the possible remedies before getting into TRT. I’ve taken testosterone enanthate only, 2 shots per week (an average of 70mg per week), for months with no AI and felt good just the first 2 weeks, to quickly going into not feeling well, but better than before. My labs were showing a free test of 27-29 pg/mL and an E2 in the 40s. Symptoms were a gynecomastia of a size of a walnut, social anxiety, crazy sweating (especially while sleeping and while working out), water retention, mild depression and irritability.
So I started with AI (I’ve tried both anastrazole and exemestane), with regular suggested doses (0.25 mg or 0.125 mg) but I’ve never managed to get dialed in and I didn’t know why at that time. It was almost one year of TRT and I still wasn’t dialed in.
It was almost time for me to get married so I decided to start with HCG (250 IU 3x week), in order to keep fertility and get the benefits Dr. Crisler was preaching about. A drug I hated since the first time I’ve tried, but I didn’t have any other choice (it doubled my gynecomastia and almost gave me a panic attack). So I decided to get a phone consultation with Dr. Crisler, asking him advices.
He told me my protocol on injecting T enanthate and HCG EOD was good (17.5 mg of T enanthate + HCG 250 IU EOD) but to switch from exemestane to anastrazole (0.125 mg at every injection).
I’ve been on this protocol for a couple of months, tapering down HCG more and more, until I crashed my E2 and learnt that I’m an AI over-responder.
So I decided to avoid touching any AI for months and I’ve been on 17.5 mg of T enanthate and 50 IU of HCG 3 x week for 3 months, and these are the results:

Total T = 1386.8 ng/dL (241 – 827 ng/dL)
Free T = 25.2 pg/mL (8.5 - 30.4 pg/mL)
Estradiol = 102.14 pg/mL (10 – 40 pg/mL)
Prolactin = 26.91 ng/mL (2.1 – 17.7 ng/mL)
TSH = 2.075 uUI/mL (0.35 – 5.5 uUI/mL)
Free T3 = 3.1 pg/mL (2.3 – 4.2 pg/mL)
Free T4 = 0.89 ng/dL (0.89 – 1.76 ng/dL)
SHBG = 23 nmol/L (10 – 80 nmol/L)
Cortisol = 16.69 ug/dL (AM: 4.3 - 22.4 ug/dL)
IGF-1 = 136.0 ng/mL (Age 31-35: 88-246 ng/mL)
DHEA-S = 209.3 ug/dL (35 – 550 ug/dL)
Pregnenolone= 211.5 ng/dL (38 – 248 ng/dL)

As you can see, despite the fact of lifting heavy 4 times x week (200 kg 6 reps of squat, 140 kg 6 reps of bench press, 170 kg 6 reps of deadlifts, 75 kg 6 resp of overhead press) and being quite muscular (180 cm, 91 kg, 11% body fat), I aromatize like a crazy and I have all the above mentioned symptoms of high E2.
I’ve booked in a phone consultation with Dr. Saya, who advised me to introduce 0.1 mg of anastrazole in the mix, along with DHEA and pregnenolone to control my anxiety (I didn’t touch pregnenolone yet, because my serum levels are already in the mid-top range).
I started conservatively and took just 0.05 mg out of a vodka solution with anastrazole, and tested E2 2 weeks after, with just one dose taken the night before the blood test.
Well, my E2 went to 46.3 pg/mL, more than halved with a single dose of 0.05 mg! I started having some libido again, the gynecomastia went completely away, my memory and focus improved, my anxiety decreased substantially and I almost stopped sweating at night.
Probably my gene expression has changed with Finasteride (as Dr. Crisler was claiming), but with people like me, with such heavy aromatization, despite having a dialed in diet and heavy workout routine, I think a really small dose of anastrazole could be a game changer.
I’m curious to know if someone else had a similar experience.

What was the total time you were off of the AI?