MESO-Rx

Anabolic Steroids

Using estradiol injection to allow for low test cycles

Sampei said:
Dunno man, I jugged a bottle that is 2 liter but was below half empty so maybe 500ml? 750ml? I may have drink 2 hours before something but not much as I injected 10IU IM of GH just to do a stupid serum test.

I'll retest without drinking anything to check if it changes by a lot or not
Click to expand...

Ah, that's definitely not enough water to skew the results by such a huge margin ...
 
verylargeshoes said:
I’d be interested to know what we SHOULD drink. Todd Lee recommends one gallon and says that people with high hematocrit are just under hydrated, but I’ve had normal hematocrit my whole life without shotgunning a gallon of water before.
Click to expand...

There is a lot of confusion about hydration and hemo parameters. Imo the confusion mostly stems from the fact that Hb and Hct are in a way relative parameters and by that I mean they are dependent on the ratio between RBC concentration and the volume of plasma. So the more plasma volume you have the lover the hemo parameters. The mistake basically stems from the fact that we are looking at Hb and Hct as solo parameters when we should be looking at them only in relation to osmolality, ie. plasma volume. To be more clear; Hb divided by "osmolality" = "real Hb", and the same for Hct. Something in those lines ... If you test for osmolality when you do your bloods, simply make a calculation (my Hb was xx at an osmolality of xy) and then it wont mater that much how much water you drank before the test. You can also include something like urine concentration (USG) ...

Imo, drinking huge amounts of water before the test makes sense only if you were dehydrated. Otherwise it's a stupid idea as you are inducing a transient increase in blood plasma which isn't representative of your normal hemo parameters. Ie. drink according to thirst.
 
Jin23 said:
There is a lot of confusion about hydration and hemo parameters. Imo the confusion mostly stems from the fact that Hb and Hct are in a way relative parameters and by that I mean they are dependent on the ratio between RBC concentration and the volume of plasma. So the more plasma volume you have the lover the hemo parameters. The mistake basically stems from the fact that we are looking at Hb and Hct as solo parameters when we should be looking at them only in relation to osmolality, ie. plasma volume. To be more clear; Hb divided by "osmolality" = "real Hb", and the same for Hct. Something in those lines ... If you test for osmolality when you do your bloods, simply make a calculation (my Hb was xx at an osmolality of xy) and then it wont mater that much how much water you drank before the test. You can also include something like urine concentration (USG) ...

Imo, drinking huge amounts of water before the test makes sense only if you were dehydrated. Otherwise it's a stupid idea as you are inducing a transient increase in blood plasma which isn't representative of your normal hemo parameters. Ie. drink according to thirst.
Click to expand...
This is the direct opposite advice if what Dr Todd Lee advises on his YouTube channel (drink lots of water before a morning blood test).

Personally I've tried both and there isn't much difference on my blood counts.
 
imo/ime being overly hydrated only skews the results, better to be at a normal fluid intake for that day of blood test to get a " more accurate" results,, Sure if you over hydrate certain markers will be improved , but not reflect what is a day to day occurance,,
 
bananafeet said:
This is the direct opposite advice if what Dr Todd Lee advises on his YouTube channel (drink lots of water before a morning blood test).

Personally I've tried both and there isn't much difference on my blood counts.
Click to expand...

@PaintDrinker tested the same day dehydrated vs hydrated and the variance was huge, like 3-4% iirc.. he'll tell you.
 
bananafeet said:
This is the direct opposite advice if what Dr Todd Lee advises on his YouTube channel (drink lots of water before a morning blood test).

Personally I've tried both and there isn't much difference on my blood counts.
Click to expand...

Who is that and should I care? That's dispensing generalized advice, and there is a difference when you're doing that, ie. saying something that will benefit the masses, vs being specific.

How much water intake impacts your plasma volume depends on how much your body is able to hold on to water, which differs a lot between individuals. HPA axis/kidneys + compounds you are on.
 
I don't want to revive and old thread.

But I came across a Dr on YT who is lowering his lipid profile while on TRT with oral estrogen.

He is at around 90pg/mL and says it's working better than an expensive statin.

Sort of makes sense. But are there any risks outside of fluid retention for super high E2? I read through that Type 2x thread but couldn't get a clear answer.

I've noticed on my own bloodwork better lipids with higher E2 levels (top of range).

I think the argument of ROS damage in the endothelium due to sythentic androgens not aromatising sort of implies the protective effects of E2. Also increased NOx production. Of course E2 is a paracrine hormone so blood levels are somewhat non indicative of tissue levels.

Any input from the brains trust?
 
verylargeshoes said:
It's unfortunate that he doesn't actually explain the reasoning and evidence behind his assertion, but just gestures at a pile of references and leaves it as an exercise for the student. The post itself was not enlightening. If anybody has done their homework on this, I'd love to hear more about it.
Click to expand...
He never does, guy claims injectable primobolan is liver toxic and then never goes into the mechanisms of action or why he believes that.

Considering all the literature on primo proves otherwise one would think he'd at least mention why he believes that.
 
I actually did a cycle years ago with no test base

EE- 5mg a week (e2 was 100pmol 3 days after injection)
Deca - 600mg a week
Mast E - 300mg a week
Dhea - 50mg daily
Preg - 25mg daily

Blood work was okey felt actually euphoric during the cycle I stopped and went back on Test as I couldn’t find any data if it can cause issues in the future once injecting exogenous E you basically cut the middle man which is the aromatization don’t know if e2 blood serum and tissue serum are different either way wouldn’t risk it with no data
Running low test with estradiol and another anabolic I have no clue what would happen and if it will cut the aromatization or maybe it will provoke it and you’ll wake up with a clit between your legs who knows..
 
verylargeshoes said:
It's unfortunate that he doesn't actually explain the reasoning and evidence behind his assertion, but just gestures at a pile of references and leaves it as an exercise for the student. The post itself was not enlightening. If anybody has done their homework on this, I'd love to hear more about it.
Click to expand...
I will try to respond to the 3 claims:

✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations

Refutation:
The study discusses synthetic or environment disruption by xenoestrogens. This doesn’t support the argument that identical exogenous estrogen is harmful. From the study:

“ As a result, low doses of xenoestrogens can interfere with natural estrogen actions, even in the presence of higher circulating E2 concentrations.”

✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]

Refutation:
This is true. More HGH may be needed to get the same IGF1 response especially when using oral E2 (first pass effect):
A Switch from Oral (2 mg/Day) to Transdermal (50 mg/Day) 17b-Estradiol Therapy Increases Serum Insulin-Like Growth Factor-I Levels in Recombinant Human Growth Hormone (GH)-Substituted Women with GH Deficiency
https://sci-hub.se/https://doi.org/10.1210/jcem.85.1.6311

“Serum IGF-I levels significantly increased after the switch from oral to transdermal estrogen therapy “

✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]

Refutation:
This is true but the study was on men with normal testosterone levels. It follows reasoning that men on exogenous testosterone would have lower levels of SHBG and the effect won’t be as dramatic.


Counter evidence:
  1. Higher levels of estrogen are associated with reduced mortality and endothelial function
  2. Man with aromatase deficiency was treated with exogenous estradiol improving various health markers (bone, lipids etc) with exogenous estrogen treatment
  3. Higher E2 is associated with better lipid profiles, lower atherosclerosis and lower cardiovascular risk. Benefits are independent of testosterone level.


Endogenous estrogen levels are associated with endothelial function in males independently of lipid levels
DOI 10.1007/s12020-010-9307-7
“Flow-mediated dilatation (FMD) and intima-media thickness (IMT) of the common carotid artery were evaluated. Obesity parameters were recorded; estradiol, testosterone, SHBG, free testosterone, insulin, as well as glucose and lipid levels were measured. FMD was positively correlated with estradiol (r = 0.201, P = 0.041) and negatively with total cholesterol (r = -0.205, P = 0.022), low density lipoproteins (r = -0.232, P = 0.009), and triglyceride levels (r = -0.179, P = 0.046). In multivariate analysis, the association of FMD with estrogen was independent of BMI and lipid levels. No significant association between FMD and testosterone levels was found.”

EFFECT OF TESTOSTERONE AND ESTRADIOL IN A MAN WITH AROMATASE DEFICIENCY
https://sci-hub.se/10.1056/NEJM199707103370204
“Estrogen treatment induced substantial decreases in the ratio of serum LDL cholesterol to serum HDL cholesterol and in serum triglycerides in our patient (Table 1). Although this effect may depend at least in part on reduced concentrations of serum testosterone, it is clear that the abnormal lipid profile in an aromatase-deficient subject can be modified with estrogen treatment.17”

“With estrogen treatment spinal bone mineral density increased, and complete epiphyseal closure was achieved after nine months. The increases in bone mineral density, serum levels of alkaline phosphatase and osteocalcin, and urinary excretion of pyridinoline were similar to those that occur during normal skeletal maturation during puberty.13,14”

Endogenous Sex Hormones and Cardiovascular Disease in Men
“Estradiol was found to be associated with apolipoprotein E (15).”

“Peripheral arterial disease To our knowledge, only one study (104) has been published on the association between endogenous sex hormones and peripheral arterial disease. The Edinburgh Artery Study, a large-scale prospective survey, found that after 5 yr of follow-up, 40 men had developed peripheral arterial disease. In a nested case-control study, total T, SHBG, and estradiol appeared to have a protective effect, whereas estrone appeared to have an adverse effect.”

“In male-tofemale transsexuals, long-term estrogen supplementation improves vascular function, compared with men [(mean se) 11.5 1.3% vs. 5.2 1.0%, respectively, P 0.005] (121). The effect of high-dose conjugated estrogen (5 mg/d) was studied in the Coronary Drug Project, but estrogen treatment was discontinued because it nearly doubled the incidence of nonfatal MI in the treatment group (122). It may be stated that estrogen as well as T administration had both beneficial and deleterious effects on cardiovascular functioning, depending on dose, population, and end point.”

Conclusion:
Exogenous supplementation in men of E2 provides the same benefits are E2 produced by aromatisation. Higher levels have been shown to be harmful (last quote).

I don't know what qualifies as "high" but maybe getting into the female reference range would be ok.

I think Type-2x is AFK, I sent him a message asking him about ROS and synthetic androgens but he didn't respond. So I'm posting it here not on the original thread.

I will defer to someone with a formal education (not myself).
 
bananafeet said:
I will try to respond to the 3 claims:

✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations

Refutation:
The study discusses synthetic or environment disruption by xenoestrogens. This doesn’t support the argument that identical exogenous estrogen is harmful. From the study:

“ As a result, low doses of xenoestrogens can interfere with natural estrogen actions, even in the presence of higher circulating E2 concentrations.”

✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]

Refutation:
This is true. More HGH may be needed to get the same IGF1 response especially when using oral E2 (first pass effect):
A Switch from Oral (2 mg/Day) to Transdermal (50 mg/Day) 17b-Estradiol Therapy Increases Serum Insulin-Like Growth Factor-I Levels in Recombinant Human Growth Hormone (GH)-Substituted Women with GH Deficiency
https://sci-hub.se/https://doi.org/10.1210/jcem.85.1.6311

“Serum IGF-I levels significantly increased after the switch from oral to transdermal estrogen therapy “

✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]

Refutation:
This is true but the study was on men with normal testosterone levels. It follows reasoning that men on exogenous testosterone would have lower levels of SHBG and the effect won’t be as dramatic.


Counter evidence:
  1. Higher levels of estrogen are associated with reduced mortality and endothelial function
  2. Man with aromatase deficiency was treated with exogenous estradiol improving various health markers (bone, lipids etc) with exogenous estrogen treatment
  3. Higher E2 is associated with better lipid profiles, lower atherosclerosis and lower cardiovascular risk. Benefits are independent of testosterone level.


Endogenous estrogen levels are associated with endothelial function in males independently of lipid levels
DOI 10.1007/s12020-010-9307-7
“Flow-mediated dilatation (FMD) and intima-media thickness (IMT) of the common carotid artery were evaluated. Obesity parameters were recorded; estradiol, testosterone, SHBG, free testosterone, insulin, as well as glucose and lipid levels were measured. FMD was positively correlated with estradiol (r = 0.201, P = 0.041) and negatively with total cholesterol (r = -0.205, P = 0.022), low density lipoproteins (r = -0.232, P = 0.009), and triglyceride levels (r = -0.179, P = 0.046). In multivariate analysis, the association of FMD with estrogen was independent of BMI and lipid levels. No significant association between FMD and testosterone levels was found.”

EFFECT OF TESTOSTERONE AND ESTRADIOL IN A MAN WITH AROMATASE DEFICIENCY
https://sci-hub.se/10.1056/NEJM199707103370204
“Estrogen treatment induced substantial decreases in the ratio of serum LDL cholesterol to serum HDL cholesterol and in serum triglycerides in our patient (Table 1). Although this effect may depend at least in part on reduced concentrations of serum testosterone, it is clear that the abnormal lipid profile in an aromatase-deficient subject can be modified with estrogen treatment.17”

“With estrogen treatment spinal bone mineral density increased, and complete epiphyseal closure was achieved after nine months. The increases in bone mineral density, serum levels of alkaline phosphatase and osteocalcin, and urinary excretion of pyridinoline were similar to those that occur during normal skeletal maturation during puberty.13,14”

Endogenous Sex Hormones and Cardiovascular Disease in Men
“Estradiol was found to be associated with apolipoprotein E (15).”

“Peripheral arterial disease To our knowledge, only one study (104) has been published on the association between endogenous sex hormones and peripheral arterial disease. The Edinburgh Artery Study, a large-scale prospective survey, found that after 5 yr of follow-up, 40 men had developed peripheral arterial disease. In a nested case-control study, total T, SHBG, and estradiol appeared to have a protective effect, whereas estrone appeared to have an adverse effect.”

“In male-tofemale transsexuals, long-term estrogen supplementation improves vascular function, compared with men [(mean se) 11.5 1.3% vs. 5.2 1.0%, respectively, P 0.005] (121). The effect of high-dose conjugated estrogen (5 mg/d) was studied in the Coronary Drug Project, but estrogen treatment was discontinued because it nearly doubled the incidence of nonfatal MI in the treatment group (122). It may be stated that estrogen as well as T administration had both beneficial and deleterious effects on cardiovascular functioning, depending on dose, population, and end point.”

Conclusion:
Exogenous supplementation in men of E2 provides the same benefits are E2 produced by aromatisation. Higher levels have been shown to be harmful (last quote).

I don't know what qualifies as "high" but maybe getting into the female reference range would be ok.

I think Type-2x is AFK, I sent him a message asking him about ROS and synthetic androgens but he didn't respond. So I'm posting it here not on the original thread.

I will defer to someone with a formal education (not myself).
Click to expand...
type 2 just wants $ for information nowadays, Thats likely why he doesn't respond, gotta make $ though,,
 
Sampei said:
So I have been thinking of a new possible approach for using some substances that are usually a bit tricky due to the lowering estrogen ability they have attached to their use so that one could use high dose of these mild compounds without having to blast test very high.

EQ and Primo are the main focus of this brainstorm idea I'm having, but Nandrolone can be another one.

So I can't run any of these two substances on a ratio of 1:1 without killing my E2.
I have noticed that both substances are great run at high dosages with minimum impacts on bloods especially EQ for me is a breeze with no side effect except those damn low E2.

I have been thinking, why not run 500mg of test as a base and then 1.5G of EQ for example and to balance E2 just inject low dosages of estradiol cypionate?

You could run a very high anabolic cycle with minimal sides and still have a healthy level of E2.

Please rip me a new one or give me your criticism/ideas on this approach.
Click to expand...
Have you tried just running HCG toghether witg it? HCG acts for me like liquid estrogen.

Without HCG i could run 700mg Test no AI without any problem. Like nothing.
With hcg even at 500mg im bitching around, my back looks like the battlefield of verdun, no appetite, cant sleep... you name it, and my estrogen EXPLODES at least thats what tge bloodworks says.

So maybe just take 300mcg of HCG every other day or 150 every day?
 
Proud Pangolin said:
Have you tried just running HCG toghether witg it? HCG acts for me like liquid estrogen.

Without HCG i could run 700mg Test no AI without any problem. Like nothing.
With hcg even at 500mg im bitching around, my back looks like the battlefield of verdun, no appetite, cant sleep... you name it, and my estrogen EXPLODES at least thats what tge bloodworks says.

So maybe just take 300mcg of HCG every other day or 150 every day?
Click to expand...
I take 500IU EOD, it barely helps
 
Think it would be a hell of a lot easier to pop 5mg of Dbol a day... LOL. That was the answer by dudes back in the day when Durabolin/Deca Durabolin and Primo ruled the roost.
 
wp_375 said:
Think it would be a hell of a lot easier to pop 5mg of Dbol a day... LOL. That was the answer by dudes back in the day when Durabolin/Deca Durabolin and Primo ruled the roost.
Click to expand...
I like this approach too but I also love dbol. The difficulties it presents are that you can't measure your e2 if that's important to you. Also although it feels the same can we be sure that methyl e2 fulfills all the same functions as e2? And some people just don't like dbol. It can raise BP
 
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