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Daz69

Old School thoughts on Estradiol

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Quite a long read, but in my opinion worth it:

 

Estradiol:

The lower amounts of both visceral (intra-abdominal) and subcutaneous fat levels one has determines to a large degree the side effects brought on by estrogen. For example one very serious misunderstanding of estrogen and its effects on adiposity are that estrogen increases fat gain or retards fat loss, when in effect the opposite is true. This is especially true when TESTOSTERONE is present. When testosterone is low or not present, estrogen can then under those circumstances create problems. Estradiol (E2), is probably a more effective fat loss aid than is testosterone. Estradiol can also prevent muscle loss, only in the presence of testosterone, by blocking the low affinity glucocorticoid receptors protecting against the effects of cortisol. This is why the top dogs ALWAYS have testosterone in the stack at high levels especially when dieting. I will go into more details of estrogen and its key rolls on a future date. I'll enlighten some very interesting information on how estrogen works as the anabolic.

 

2: Some people advocate low test to control estrogen, and other such as myself recommend higher test amounts. What is the role of testosterone, estrogen and diet. How do then influence each other. Do they work differently in a calorie rich vs a low calorie, higher stress environment. Does low test work better then high test at removing body fat?

There is a CONSTANT and CONTINUAL run of high amount of test through most or all bodybuilding competitors regimes. This high base is run up all the way until the last few weeks. The only changes to test are the esters. Faster ones are brought in closer to show time. Why, and what does it have to do with estrogen?

Both muscle and fat tissue metabolize free estrogen, estrone and estradiol. Through the aromatase enzyme, estrogen is actually produced in BOTH your fat and muscle cells via testosterone. That conversion to estrogen could happen in either your fat cells or muscle cells which plays a big role in the production of good or bad estrogen metabolites. This is the reason we pound the table to grow from a lean stage. The leaner the better. We want more E2 produced via muscle tissue vs fat. Every single hormone plays an ever important role all by itself and yet the production of each subsequent specific hormone is dependent on the other hormones.

I mentioned earlier  estrogen, specifically estradiol (E2), is probably a more effective fat loss aid than is testosterone. But with one very important caveat. An increase in estradiol must be accompanied by an equal or larger increase in testosterone if we are reap the positive effects on both fat loss and muscle retention. Testosterone increases IGF-1, while estradiol prolongs the half-life and effect of the hormone by increasing IGFBP-3 and IGF1-receptor density.

One key to understand, estrogen is not present to promote skeletal muscle hypertrophy, but rather to prevent atrophy especially in calorie restricted environments. Also excessive estrogen can and will work against you in different ways especially in a calorie surplus environment with high body fat levels. In a second mechanism estradiol prevent muscle loss, once again only in the presence of test by blocking glucocorticoid receptors protecting against the effects of cortisol.

Estrogen also plays another role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation. More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to enhance recovery when needed. Estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window.

Besides muscle tissue, estrogen also stabilizes muscle membranes and diminishes sarcolemmal disruption. In other words estrogen acts to reduce exercise-induced muscle damage and inflammatory responses by acting as both as an strong antioxidant against exercise-induced membrane phospholipid peroxidation and also acts as a cholesterol-like influence on membrane fluidity and stability.

So what is the bottom line. Higher test levels produce E2 which helps the bodybuilder remain fuller and RETAIN more structural tissue especially when dieting. E2 also keeps the muscle's structural membrane intact, which keeps the cells better hydrated and anabolic. And as you can see it also plays a big role in muscle energy recovery too.

So now that we know this, I will ask these few questions. What is your goal when dieting? Further more, what is the goal of those giving advise on low test while dieting. They may be VERY different. Those running lower test FIRST PRIORITY is not the maximum retention of muscle and strength, but the extreme removal of body fat. When I diet down, my FIRST AND PRIMARY goal is muscle retention, followed by fat loss. For others it may be backwards. What most forget, and I'll say it again, those bodybuilders from the past who ran low test, made up the loss of estrogen with running high aromatizing orals. Remember that!!!!! Its has been said over and over again, running 100mg plus a day of Dbol in the 70's was the norm for the top echelon. And that is just the orals......

You may have also importantly noticed in the Pro's steroid cycle link, deca and eq, were also run concurrently, not the tren/mast combination, most are use to hearing about in final 12 or so weeks leading into a show. This goes completely against what many are preaching here. Again, why run deca as far into competition mode as possible. We will once again revisit the top goal of the competitor, the retention of lean tissue during calorie restriction mode.

We can take a history lesson as to why deca is used in this phase. The main reason for Nandrolone?s widespread use and popularity is owed in large part to the fact that it was essentially the second officially created and marketed anabolic steroid to ever be made (1957) after dianabol (1955). NPP was created first, but due to the short half live and too frequent of injections for patients, deca the longer version was brought to market. Nandrolone Decanoate, saw a vast and wide range of medical uses ranging from the promotion of weight and lean mass in patients with wasting diseases to the treatment of burn victims, geriatric patients, anemia, and even for the treatment of child growth and development disorders. It is extremely effective and safe bringing up the lean body-weight of patients but is also has benefits for their impaired immune systems too.

Think about it this way, say you have a patient with severe burns whose metabolic and calorie needs are not only through the roof, but at the same time they are unable to eat. Calorie consumption is completely impaired and the body begins to eat itself alive. How do you stabilize the body-weight without adding additional stress to an already compromised and failing body systems (heart, liver and kidneys). Yes, this is what deca was designed for. For those of you with a general understanding of this situation, do you think you could put the same patient on tren? What would be the outcome of that same deathly ill patient on tren? Even some of the latest HIV studies show deca therapy, even in the absence of an exercise program in borderline hypo-gonadal men caused substantial nitrogen retention compared with placebo, similar in extent to the nitrogen retention previously achieved with GH.

So deca is ALSO a POWERFUL anti-catabolic especially when calories are restricted. Furthermore, the second reason deca is run as far into prep as possible is the fluid it brings into the joints during this critical stage. Remember the astronaut example, where regardless of hormones, vitamins, and minerals provided, bone mass diminishes as the loads lighten in space due to zero gravity. The same premise works here too. If your joints hurt and you are now moving lighter weight due to the pain, the body WILL also make adjustments to lean tissue reserves. You want the same loads placed on the system for as long as possible. Deca makes this possible!!!!!!!!!!!!

I will leave you with this thought. Imagine you have a very dirty car full of mud and dirt. You have soap, water, towels and wax to clean detail the paint. Why could you not just leave out the soap and water out and just wax the car straight? The car in the end would look the same. Why yes, waxing a dirty car would clean the car but damage the paint. You would want the surface to be clean FIRST prior to the addition of wax. Many bodybuilders, including myself consider tren, halo, winstrol the wax, and only use it when they are "clean" or devoid of fat to prevent additional stress and damage it creates. They are used as a final tool to bring out those extreme details, like the wax.

Test and deca are the dieting lifeblood, just like the soap and water is to that dirty "fat" car......

 

DrX...

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On 9/9/2017 at 8:23 PM, Daz69 said:

 


Both muscle and fat tissue metabolize free estrogen, estrone and estradiol. Through the aromatase enzyme, estrogen is actually produced in BOTH your fat and muscle cells via testosterone. That conversion to estrogen could happen in either your fat cells or muscle cells which plays a big role in the production of good or bad estrogen metabolites. This is the reason we pound the table to grow from a lean stage. The leaner the better. We want more E2 produced via muscle tissue vs fat. Every single hormone plays an ever important role all by itself and yet the production of each subsequent specific hormone is dependent on the other hormones.

Hi Daz,

 

Interesting read. What are the differences between the aromatase in myocytes vs adipose tissue? And what are "good" estrogen metabolites as opposed to "bad" ones?

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On ‎11‎/‎1‎/‎2017 at 10:20 AM, tomleegolf said:

Hi Daz,

 

Interesting read. What are the differences between the aromatase in myocytes vs adipose tissue? And what are "good" estrogen metabolites as opposed to "bad" ones?

 

Aromatase is aromatase, any change and it ceases to be the same molecule, did you mean aromatization in myocytes as opposed to adipose tissue..?

 

Regards estrogen metabolites, there are those that trigger a positive effect as opposed to those that trigger negative effect, such as creating R.O.S that damage tissue and disrupt cellular processes..

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On 11/2/2017 at 2:22 PM, Daz69 said:

 

Aromatase is aromatase, any change and it ceases to be the same molecule, did you mean aromatization in myocytes as opposed to adipose tissue..?

 

Regards estrogen metabolites, there are those that trigger a positive effect as opposed to those that trigger negative effect, such as creating R.O.S that damage tissue and disrupt cellular processes..

Yeah, that's what I meant. I thought maybe there were a group of aromatase enzymes, like there are groups of aldehyde dehydrogenases or glucose transporters, which have slightly different properties but all serve the same function.

 

If there is just one aromatase enzyme, then why is it that aromatisation in adipocytes results in harmful metabolites while not in myocytes? What are some examples of metabolites that would occur in each tissue?

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19 hours ago, tomleegolf said:

Yeah, that's what I meant. I thought maybe there were a group of aromatase enzymes, like there are groups of aldehyde dehydrogenases or glucose transporters, which have slightly different properties but all serve the same function.

 

If there is just one aromatase enzyme, then why is it that aromatisation in adipocytes results in harmful metabolites while not in myocytes? What are some examples of metabolites that would occur in each tissue?

 

Whilst the pathway from testosterone and androstenedione use cyp19a1 (aromatase), to synthesise estrone and estradiol, there is a reverse pathway between estrone and estradiol that uses 17-beta HSD.. 

 

Quote

why is it that aromatisation in adipocytes results in harmful metabolites while not in myocytes? What are some examples of metabolites that would occur in each tissue?

Google..

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