Boosting Test-E dosage Mid-Cycle?

[Saitama0851]

What do ya'll think of this cycle:

* Test-E 300mg/wk - Weeks 1-8
* Dbol 25mg ED - Weeks 2-5
* Increase Test-E dose to 600mg/wk - Weeks 9-16
* Aromasin 12.5mg e3d starting on 3rd pin (week 2) and adjusting dose/timing for sides/bloating
* Nolva on deck for gyno
* PCT: Nolva 25/25/25/25/25 starting 2 weeks after last test shot

[cousinmuscles]

Take exemestane twice per day at 12,5-25mg per day depending on bloods. Read this: https://forums.steroid.com/anabolic-...rdosed-ai.html

Run your cycle for 12 weeks at the same dose . If it's your first cycle use test only. Add clomid to PCT. Add HCG throughout the cycle 250iu twice per week until a couple days before you start PCT. Read this too: https://forums.steroid.com/anabolic-...rst-cycle.html

Welcome to the forum

[Saitama0851]

Thank you for the welcome! I will add clomid to the PCT and will try to source the HCG soon. Can I start HCG a month into the cycle?

I just read over your article on aromasin (exemestane). So from what I understand, even a higher dose will not crash my estrogen? Suicidal AI's are exaggerated in their potential to crash estrogen in males? Many people over on other sites have mentioned crashed estrogen being as bad as higher estrogen. So to begin the cycle I can start at a 12.5-25 ED dose and adjust? I was told to start at 12.5 e3d and dial it from there once sides start or don't start (because estrogen is actually good/necessary in the right amt correct?)

I also have another question - can you speak a little about (in your personal experience) what sides to look for when the current AI dose is ineffective? Can one still be taking the AI enough to counteract excessive physical sides (itchy nips, bloating/water) but still have high estrogen levels only detectable via bloods?

[cousinmuscles]

Thank you for the welcome! I will add clomid to the PCT and will try to source the HCG soon. Can I start HCG a month into the cycle?

I just read over your article on aromasin (exemestane). So from what I understand, even a higher dose will not crash my estrogen? Suicidal AI's are exaggerated in their potential to crash estrogen in males? Many people over on other sites have mentioned crashed estrogen being as bad as higher estrogen. So to begin the cycle I can start at a 12.5-25 ED dose and adjust? I was told to start at 12.5 e3d and dial it from there once sides start or don't start (because estrogen is actually good/necessary in the right amt correct?)

I also have another question - can you speak a little about (in your personal experience) what sides to look for when the current AI dose is ineffective? Can one still be taking the AI enough to counteract excessive physical sides (itchy nips, bloating/water) but still have high estrogen levels only detectable via bloods?

Not my article Yes it is pretty difficult to crash your estrogen with exemestane I haven't managed to do it on cycle...

Why higher serum estrogen levels? Have a look:

Am J Med. 1982 Dec;73(6):872-81.
Serum estrogen levels in men with acute myocardial infarction.
Klaiber EL, Broverman DM, Haffajee CI, Hochman JS, Sacks GM, Dalen JE.
Serum estradiol and serum estrone levels were assessed in 29 men in 14 men in whom myocardial infarction was ruled out; in 12 men without apparent coronary heart disease but hospitalized in an intensive care unit; and in 28 men who were not hospitalized and who acted as control subjects. (The 12 men who were hospitalized but who did not have coronary heart disease were included to control for physical and emotional stress of a severe medical illness.) Ages ranged from 21 to 56 years. Age, height, and weight did not differ significantly among groups. Blood samples were obtained in the patient groups on each of the first three days of hospitalization. The serum estrone level was significantly elevated in all four patient groups when compared with that in the control group. Estrone level, then, did not differentiate patients with and without coronary heart disease. Serum estradiol levels were significantly elevated in the groups with myocardial infarction, unstable angina, and in the group in whom myocardial infarction was ruled out. However, estradiol levels were not significantly elevated in the group in the intensive care unit without coronary heart disease when compared to the level in the normal control group. Serum estradiol levels, then, were elevated in men with confirmed or suspected coronary heart disease but were not elevated in men without coronary heart disease even under the stressful conditions found in an intensive care unit. Serum estradiol levels were significantly and positively correlated (p less than 0.03) with serum total creatine phosphokinase levels in the patients with myocardial infarction. The five patients with myocardial infarction who died within 10 days of admission had markedly elevated serum estradiol levels. The potential significance of these serum estradiol elevations is discussed in terms of estradiol’s ability to enhance adrenergic neural activity and the resultant increase in myocardial oxygen demand.

Lancet. 1976 Jul 3;2(7975):14-8.
Evidence for hyperoestrogenaemia as a risk factor for myocardial infarction in men.
Phillips GB.
Fifteen men who had had a myocardial infarction between the ages of 32 and 42 years were compared with fifteen age-matched healthy men. Seven of the patients had a strikingly slow rate of beard growth, three had evidence of gynaecomastia, and three had a loss of libido. The slow beard growth and decreased libido, and possibly the gynaecomastia, preceded the myocardial infarction. Mean serum oestradiol and oestrone concentrations were significantly increased in the patients, 43.5 +/- 8.8 (standard deviation) and 50.7 +/- 9.5, respectively, compared wth 33.5 +/- 5.5 and 37.5 +/- 5.8 pg/ml in the controls (p less than 0.001). Mean serum testosterone and dihydrotestosterone concentrations were not significantly different in the two groups. Serum oestradiol and oestrone concentrations were directly proportional to each other as were those of testosterone and dihydrotestosterone. These results suggest that the hyperoestrogenaemia preceded the myocardial infarction and that hyperoestrogenaemia may be an important risk factor for myocardial infarction in men.

Arch Intern Med. 1982 Jan;142(1):42-4.
Relationship between sex hormones, myocardial infarction, and occlusive coronary disease.
Luria MH, Johnson MW, Pego R, Seuc CA, Manubens SJ, Wieland MR, Wieland RG.
An alteration in sex hormones has been considered a risk factor for myocardial infarction. In this study, estradiol (E2) and testosterone (T) levels were evaluated in healthy firefighters, patients with myocardial infarction acutely and during their convalescence, patients with no evidence of occlusive coronary artery disease on arteriography, and patients with chronic angina pectoris in whom there was at least one vessel that indicated 50% occlusive coronary artery disease. Although T levels were similar in all groups, E2 levels were substantially higher in patients with myocardial infarction and in patients with chronic angina pectoris. These results support the hypothesis that elevated estrogen levels may be a risk factor for myocardial infarction and coronary artery disease, possibly by promoting clotting or coronary spasm.

Arteriosclerosis, Thrombosis, and Vascular Biology. 1996; 16: 1383-1387
The Association of Hyperestrogenemia With Coronary Thrombosis in Men
Gerald B. Phillips; Bruce H. Pinkernell; Tian-Yi Jing
Both hyperestrogenemia and hypotestosteronemia have been reported in association with myocardial infarction (MI) in men. It was previously observed that the serum testosterone concentration correlated negatively with the degree of coronary artery disease (CAD) in men who had never had a known MI. The present study investigated the relationship of sex hormone levels to the thrombotic component of MI by comparing these levels in 18 men who had had an MI (ie, thrombosis) and 50 men with no history of MI (ie, no thrombosis) whose degree of CAD was in the same range. The mean degree of CAD, age, and body mass index in these two groups was not significantly different. The mean serum estradiol level in the men who had had an MI (38.5±8.8 pg/mL) was higher (P=.002) than the level in the men who had not had an MI (31.9±7.1 pg/mL). The mean levels of testosterone, free testosterone, sex hormone–binding globulin, insulin, dehydroepiandrosterone sulfate, cholesterol, HDL cholesterol, and systolic and diastolic blood pressure did not differ significantly. Estradiol was the only variable measured that showed a significant relationship to MI (P<.003 by multivariate logistic regression). These findings suggest that hyperestrogenemia may be related to the thrombosis of MI.

Am J Med. 1983 May;74(5):863-9.
Association of hyperestrogenemia and coronary heart disease in men in the Framingham cohort.
Phillips GB, Castelli WP, Abbott RD, McNamara PM.
The serum levels of estradiol and testosterone as well as established risk factors for coronary heart disease were estimated in 61 men (mean age 70.0 +/- 6.4 [SD] years) with coronary heart disease and in 61 matched control subjects enrolled in the Framingham Heart Study. The mean serum estradiol level was significantly higher in the subjects with coronary disease (p = 0.011). This difference in estradiol level increased with the exclusion of subjects older than 75 years (p less than 0.001). The mean serum testosterone level was not significantly different. None of the established risk factors for coronary heart disease was different between subjects with coronary disease and control subjects except blood glucose level, which was higher in the subjects with coronary disease (p = 0.025). We conclude that hyperestrogenemia is an important correlate of coronary heart disease in men.

Neurology. 2007 Feb 20;68(8):563-8.
Serum estradiol and risk of stroke in elderly men.
Abbott RD1, Launer LJ, Rodriguez BL, Ross GW, Wilson PW, Masaki KH, Strozyk D, Curb JD, Yano K, Popper JS, Petrovitch H.
Author information
Abstract
OBJECTIVE:
To determine if levels of serum estradiol and testosterone can predict stroke in a population-based sample of elderly men.

METHODS:
Serum 17beta estradiol and testosterone were measured in 2,197 men aged 71 to 93 years who participated in the Honolulu-Asia Aging Study from 1991 to 1993. All were free of prevalent stroke, coronary heart disease, and cancer. Participants were followed to the end of 1998 for thromboembolic and hemorrhagic events.

RESULTS:
During the course of follow-up, 124 men developed a stroke (9.1/1,000 person-years). After age adjustment, men in the top quintile of serum estradiol (> or =125 pmol/L [34.1 pg/mL]) experienced a twofold excess risk of stroke vs men whose estradiol levels were lower (14.8 vs 7.3/1,000 person-years, p < 0.001). Among the lower quintiles, there were little differences in the risk of stroke. Findings were also significant and comparable for bioavailable estradiol and for thromboembolic and hemorrhagic events. After additional adjustment for hypertension, diabetes, adiposity, cholesterol concentrations, atrial fibrillation, and other characteristics, men in the top quintile of serum estradiol continued to have a higher risk of stroke vs those whose estradiol levels were lower (relative hazards = 2.2; 95% CI = 1.5 to 3.4, p < 0.001). Testosterone was not related to the risk of stroke.

CONCLUSIONS:
High levels of serum estradiol may be associated with an elevated risk of stroke in elderly men.

There are studies showing low testosterone with high estrogen correlates with cardiovascular issues, and normal test with high estrogen same thing. Even low test but that's a different issue.

Before I knew this in my first cycle I tried going without an AI. By the time the test had kicked in I just got bloated, looked fat, my BP was trickling up. I am not gyno prone it seems. Got acne issues which only got worse with both test and higher estrogen. Who knows what happened on the insides lol. When I started using the exemestane my libido got much better and the acne stopped increasing. What I felt most beneficial with FREQUENT intake of exemestane (twice per day) was the acne. On my second cycle I didn't see any increase in acne on vs off cycle... took exemestane twice daily 6.25mg each time. So I am guessing it is best to take into account its short half life and keep estrogen levels stable. My e2 pre cycle was 29 pg/ml or so, on 600mg test and 12.5mg exemestane it was 30 pg/ml. Visual sides and how you see are one thing, but you need hard data to know what may be going on inside of you. Is one cycle enough for you? Having read the above data how would you choose to do it?

There's lots of talk about high estrogen being needed for growth but I haven't been convinced. There was a thread kind of recent with some guy who took 600mg no AI for a while and started going bald, grey hair et.c. You can reverse/have surgery for gyno but grey hair lol won't be nice. It is also harder to recover and PCT from a cycle if you don't manage estrogen. There is also another recent thread where some guy took 1mg arimidex daily right off the start of a beginner cycle and got erectile dysfunction within days lol.

[GearHeaded]

I just read over your article on aromasin (exemestane). So from what I understand, even a higher dose will not crash my estrogen? Suicidal AI's are exaggerated in their potential to crash estrogen in males? Many people over on other sites have mentioned crashed estrogen being as bad as higher estrogen. So to begin the cycle I can start at a 12.5-25 ED dose and adjust? I was told to start at 12.5 e3d and dial it from there once sides start or don't start (because estrogen is actually good/necessary in the right amt correct?)

I also have another question - can you speak a little about (in your personal experience) what sides to look for when the current AI dose is ineffective? Can one still be taking the AI enough to counteract excessive physical sides (itchy nips, bloating/water) but still have high estrogen levels only detectable via bloods?

you may NOT crash your estrogen , BUT there is no benefit to starting a cycle and using too much AI and having your Testosterone levels elevate at the same time your Estrogen levels are coming down. as test goes up E is supposed to go up as well. you need to maintain a good RATIO of test to E.
simply starting a cycle out and running an AI from day one will generally screw up your ratio and keep your E too low . and you need Estrogen to grow and build muscle.

personally. I would run a very moderate dose of Test. 400mg. then see how you feel, then get blood work at 5 weeks and get your levels check. Then if you really NEED to run an AI start using one at a moderate dosage. but to take one from day one (without having past cycle experience and self knowledge and blood work) , is just more then likely going to lower your E too much and keep your E coming down as test goes up (which may cause a host of hormonal negative side effects).

if your dead set on going by the status quo you see on forums and running an AI no matter what. at least wait a few weeks into your cycle that way you give time for your test/estrogen levels to raise together and equal out. and also run a really low dose. blasting an AI from day one is just asking for trouble, and lack of gains

[Saitama0851]

Thanks for your reply GearHeaded. So I've decided to start 12.5 e3d (seems like a low enough amount based on both sides given) from the 3rd pin, get my bloods done week 5 and adjust the dose from there based on sides/values. I think this is safe because I don't want to be that special snowflake that finds out they grow tits like its cool.

Is it true that the better shape you are in already at the start (low bf, high muscle mass) that the cycle will go better?

[Saitama0851]

Thanks for your reply GearHeaded. So I've decided to start 12.5 e3d (seems like a low enough amount based on both sides given) from the 3rd pin, get my bloods done week 5 and adjust the dose from there based on sides/values. I think this is safe because I don't want to be that special snowflake that finds out they grow tits like its cool. No history of puberty gyno tho.

Is it true that the better shape you are in already at the start (low bf, high muscle mass) that the cycle will go better?

[Couchlockd]

you can start huh any time you want. you can do anything you want.

there is no rules here. its on,you.

now should you do something or not is different story.

there are generally accepted protocols that you should use as a basepoint to customize your own cycle.

I for one used to follow the eod dosing of anastrozole. I didn't know better, and it was my first cycle, so didn't know how I was supposed to feel.

this time around, I'm going e3d with anastrozole.

feel 100x better and am much fuller and sex organs work better.

research and try to understand what your reading, so you can make informed choices and be aware.