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FAQ-Aromatase for NBE
#31
Maca will raise T as well. :-)
"Veganism is not about giving anything up or losing anything; it is about gaining the peace within yourself that comes from embracing nonviolence and refusing to participate in the exploitation of the vulnerable"
~ Gary L. Francione
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#32
(21-05-2014, 03:04 PM)peggy Wrote: Maca will raise T as well. :-)


Thanks Peggy.

Wink


♦NBE Formula→Free Testosterone→5 alpha inhibitors→Aromatase→E1/E2....DNA→RNA→Protein ♦
♦Regulation of Estrogen & Progesterone-Hypothalamus→GnRH→Pituitary→FSH→Follicle→Estrogens ♦
♦ego cogito, ergo sum TG.
 Reply
#33
(20-05-2014, 03:11 PM)AnnieBL Wrote: Lotus, Lovely,

You are both right, Lovely etymologically and Lotus in terms of popular usage. Smile in and sharing the same habitation such that there is an enduring interdependence.


Thank you AnnieBL.
I think you're right. We could both be right, in how the term xenoestrogen is commonly used and its definition. There are not a lot of reliable sources to say what is the case. There is potential for when there is little information out, for definitions to get lumped together, or expanded. I'll agree that Lotus and I have a different belief of what the word means. I can't solidly prove its definition with a reliable source. I apologize to Lotus for the debate. It was argument about word definition and not about physiological function.
I've contributed a lot to herbal breast enhancement research. Check out my threads and free for personal use ebook.

The information is free and not behind paywalls.
 Reply
#34
T is essential for functions of both genders. (perhaps just free T?). It's also produced by the adrenal glands, and is responsible for height growth in both genders. Probably, the baseline of T is normal, and should just stay the same? Free T if I remember right can be converted into other hormones, and dht can't. so far it seems that dht is the one that needs to be lowered? dht is essential for early years, but in adults, I see mostly unwanted effects from it.
I've contributed a lot to herbal breast enhancement research. Check out my threads and free for personal use ebook.

The information is free and not behind paywalls.
 Reply
#35
(21-05-2014, 08:32 PM)lovely11 Wrote:
(20-05-2014, 03:11 PM)AnnieBL Wrote: Lotus, Lovely,

You are both right, Lovely etymologically and Lotus in terms of popular usage. Smile in and sharing the same habitation such that there is an enduring interdependence.


Thank you AnnieBL.
I think you're right. We could both be right, in how the term xenoestrogen is commonly used and its definition. There are not a lot of reliable sources to say what is the case. There is potential for when there is little information out, for definitions to get lumped together, or expanded. I'll agree that Lotus and I have a different belief of what the word means. I can't solidly prove its definition with a reliable source. I apologize to Lotus for the debate. It was argument about word definition and not about physiological function.


No apologizes needed, I love a good debate! Big Grin

Honestly I'd be more interested in hearing about you, like male/female?, age, your history with wiki and how long have you been researching for?

Is NBE in your future?, etc!

So, come on now don't be shy!. Wink


♦NBE Formula→Free Testosterone→5 alpha inhibitors→Aromatase→E1/E2....DNA→RNA→Protein ♦
♦Regulation of Estrogen & Progesterone-Hypothalamus→GnRH→Pituitary→FSH→Follicle→Estrogens ♦
♦ego cogito, ergo sum TG.
 Reply
#36
(21-05-2014, 08:40 PM)lovely11 Wrote: T is essential for functions of both genders. (perhaps just free T?). It's also produced by the adrenal glands, and is responsible for height growth in both genders. Probably, the baseline of T is normal, and should just stay the same? Free T if I remember right can be converted into other hormones, and dht can't. so far it seems that dht is the one that needs to be lowered? dht is essential for early years, but in adults, I see mostly unwanted effects from it.


DHT is public enemy number one for boob growth, roughly 98% of Total T is not active, and out of that 2% is what's considered Free T (bio-active). Once Free T is converted to DHT it can't convert back to Free T.

We also know that too much E turns off those receptors and feedback is locked, so what to do?.

Well you have to think in terms of reactivating those receptors, you know!!, clear them out to start the process over,

Question- what's the half life of E (not miroestriol)...does anybody get where this is going?. Wink



♦NBE Formula→Free Testosterone→5 alpha inhibitors→Aromatase→E1/E2....DNA→RNA→Protein ♦
♦Regulation of Estrogen & Progesterone-Hypothalamus→GnRH→Pituitary→FSH→Follicle→Estrogens ♦
♦ego cogito, ergo sum TG.
 Reply
#37
[/quote]
DHT is public enemy number one for boob growth, roughly 98% of Total T is not active, and out of that 2% is what's considered Free T (bio-active). Once Free T is converted to DHT it can't convert back to Free T.

We also know that too much E turns off those receptors and feedback is locked, so what to do?.

Well you have to think in terms of reactivating those receptors, you know!!, clear them out to start the process over,

Question- what's the half life of E (not miroestriol)...does anybody get where this is going?. Wink
[/quote]

I have often wondered the same thing! I think its crucial to metabolize these active hormones efficiently or they will build up in the liver much sooner than they normally do, causing the receptors to shut down/ feedback loop effect. For ex, as much as DIM is apart of men's formulas and women's to rid E excess, I think the most important part of what we need from it is actually being able to use these hormones as they flush out of the system. The liver is so important in nbe and metabolizing hormones. The abundance of free running hormones in the blood can be from poor liver function.

I think that is why the Cycling of "hormones" format is so important. It creates the re sensitivity factor consistently. I'm starting to think this is why plateaus happen after a while, loaded receptors and acute poor functioning of the liver.

This totally explained why my first attempt in nbe went detrimental. I had blood tests confirm free high estrogen and testosterone ( from high DHEA) and progesterone (though lowest of them all). And of course, I got some serious androgen conversion. I had no nbe success at all and the worst bumpy skin after months of taking all sorts of herbs (mainly estrogenic).So one can have high levels of E hormones and have no breast developmental effects at all, yet have mild masculating effects . I sadly developed some nice little stray hairs on my areola that were never there beforeSad
They were gone thankfully after cleansingBig Grin months in.

Im convinced, that DHT is the little devil that breaks nbe success. I would personally like to raise my T levels as I am naturally low, but I am so sensitive to DHT conversion from my wonky adrenals.

Starting size before NBE: Full A
2013: Full C/Small D Goal: 36-22-36.
Currently: 32DD 36" 24" 36.5"


http://www.breastnexus.com/showthread.php?tid=17332

 Reply
#38
answering:
I'm early 30's,
not inbetween gender,
researching literature no more than 3 years,
not doing nbe
I've contributed a lot to herbal breast enhancement research. Check out my threads and free for personal use ebook.

The information is free and not behind paywalls.
 Reply
#39
Thanks Lotus for the posts. I now see that you were answering our posts, but I at least wasn't seeing this. Blush. Mind you, I'm still trying to wrapt my mind around the various implications. From what you or your links say, extremely low SHBG levels are possible in conjunction with extremely low T levels, and if the results of my recent hormone level tests were reported correctly to me, my T was <0.7 and my SHBG <1.0. I suspect that in each case these readings represented 'lower than the lowest our lab can detect' which may be why no free T was calculated. They are presumably values on the Canadian or European scale, but even if multiplied up to the US scale are still abnormally low for people of either sex, in effect off the bottom of the scale. My NP does not wish to prescribe me T because of my heart condition. Despite the low levels, I suspect that PM is keeping me feeling good. PM is such a complex substance, and considered in Thailand to be beneficial for men as well as women, that it occurs to me to wonder whether it might contain androgenic as well as estrogenic components. Nothing in endocrinology ever seems to be straightforward. Huh

All the very best from
Annie

"Experience is what you have just after you needed it most"
 Reply
#40
(21-05-2014, 11:09 PM)tibetan113 Wrote:
(21-05-2014, 09:45 PM)Lotus Wrote: DHT is public enemy number one for boob growth, roughly 98% of Total T is not active, and out of that 2% is what's considered Free T (bio-active). Once Free T is converted to DHT it can't convert back to Free T.

We also know that too much E turns off those receptors and feedback is locked, so what to do?.

Well you have to think in terms of reactivating those receptors, you know!!, clear them out to start the process over,

Question- what's the half life of E (not miroestriol)...does anybody get where this is going?. Wink


I have often wondered the same thing! I think its crucial to metabolize these active hormones efficiently or they will build up in the liver much sooner than they normally do, causing the receptors to shut down/ feedback loop effect. For ex, as much as DIM is apart of men's formulas and women's to rid E excess, I think the most important part of what we need from it is actually being able to use these hormones as they flush out of the system. The liver is so important in nbe and metabolizing hormones. The abundance of free running hormones in the blood can be from poor liver function.

I think that is why the Cycling of "hormones" format is so important. It creates the re sensitivity factor consistently. I'm starting to think this is why plateaus happen after a while, loaded receptors and acute poor functioning of the liver.

This totally explained why my first attempt in nbe went detrimental. I had blood tests confirm free high estrogen and testosterone ( from high DHEA) and progesterone (though lowest of them all). And of course, I got some serious androgen conversion. I had no nbe success at all and the worst bumpy skin after months of taking all sorts of herbs (mainly estrogenic).So one can have high levels of E hormones and have no breast developmental effects at all, yet have mild masculating effects . I sadly developed some nice little stray hairs on my areola that were never there beforeSad
They were gone thankfully after cleansingBig Grin months in.

Im convinced, that DHT is the little devil that breaks nbe success. I would personally like to raise my T levels as I am naturally low, but I am so sensitive to DHT conversion from my wonky adrenals.



Hi Tibetan,

Thank you-Brilliant!!,

I wish we focused on what you just posted more often, there's so many things out there that's robbing breast growth these days. Xeno-hormones comes to mind, but this statement struck me, matter of fact the whole article did. Wink

The good estrogen causes no damage and drives immediately to the colon or to the bladder where it leaves the body. The bad estrogen backfires, gets stuck in reverse, and speeds back to the breast where it wreaks havoc. If this bad estrogen finds a parking spot on a breast cell, it will rapidly speed up cell division. If you have a lot of bad estrogen in your body, your risk of breast cancer goes up significantly.

Ok the rest of this is a read, but I think it's very important and won't (shouldn't) harm the brain, so press on my pretties. Tongue
Quote:Okay, with this understanding of all the different kinds of estrogen, lets look at how estrogen is processed within the body. Understanding how estrogen is produced, used, broken down and eliminated by your body – the estrogen pathway - is important. It will help you to understand the protocol better and make choices that support your optimum level of wellness.

I am going to quote Christine Horner, M.D. directly, from her book, Waking the Warrior Goddess, (which I highly recommend.) She has an analogy that is very simple and easy to understand.

"To understand the estrogen pathway better, lets use the analogy of a car ride. Your trip begins in the ovaries where estrogen is made and then is released into the blood. The blood vessels are like highways and estrogen flows through these blood vessel highways to get to its target destinations. When estrogen travels in the blood, it either travels alone or is attached to a substance called a "protein binder" (HSBG, Human Sex Binding Globulin), -the difference between driving alone and carpooling. When you carpool in certain cities, you can use a special high-speed lane, usually on the far left. In this lane, you can't exit from the highway. If you're driving alone, you can't use these high-speed lanes. You must travel in lanes that have access to exit lanes. Like the person driving alone, only the estrogen that travels alone – without a protein binder, SHBG – can exit from the blood-vessel highway. In this case, we are concerned about the off-ramp for only one destination: the breast tissue.

When estrogen reaches the breast, it looks for a place to "park". Parking spaces represent the "estrogen receptors", which estrogen binds to on the breast cell membranes. There are estrogen receptors all over your body, but the highest concentrations are found in the uterus and breast. Because of the relatively large number of estrogen receptors in these tissues, they respond more to estrogen than the other tissues in the body do.

When estrogen binds to an estrogen receptor, it "turns it on". A turned-on receptor causes cells to start dividing. Estrogen receptors don't turn on like a simple on/off switch. Instead, they turn on like a rheostat, a light switch with a dimmer.

The rate at which cells divide in response to estrogen is affected by many factors. First, the rate depends on the strength of the estrogen. There are strong estrogens (ESTRADIOL, ESTRONE, XENOHORMONES) and weak estrogens (ESTRIOL, PHYTOESTROGENS). Strong estrogens speed up cell division and therefore, increase the risk of cancer. Weak estrogens slow down cell division, therefore reducing the risk for cancer.

Parking at an estrogen receptor causes a lot of wear and tear on the estrogen. After awhile, it needs to go in for service. So, the estrogen leaves the estrogen receptor and heads for the liver (service station). The liver is the great detoxifier of the body. It breaks down toxins and other natural substances to prepare them for elimination.

Estrogen is broken down in the liver, and is influenced by the presence of certain chemicals. It is either broken down into a "good" kind of estrogen (Technically known as 2-hydroxyestrone) or a "bad" kind of estrogen (16-alpha hydroxyestrone). For instance substances in cruciferous vegetables and flax create more of the good kind, while environmental toxins (xenohormones) create more of the bad kind. The difference between good and bad estrogen is that good estrogen causes the cells to divide very slowly, whereas bad estrogen causes them to divide rapidly. Bad estrogen can also cause mutations or mistakes in how the cells grow that increase your risk of cancer even more.

The good estrogen causes no damage and drives immediately to the colon or to the bladder where it leaves the body. The bad estrogen backfires, gets stuck in reverse, and speeds back to the breast where it wreaks havoc. If this bad estrogen finds a parking spot on a breast cell, it will rapidly speed up cell division. If you have a lot of bad estrogen in your body, your risk of breast cancer goes up significantly.

In the colon, estrogen is either eliminated or absorbed back into the blood. If it is absorbed back into the blood, it adds to the total amount of estrogen in your body, and therefore, adds to your risk. There is a simple solution: eat more fiber. Fiber binds to the estrogen in your colon and eliminates it."

I would like to add a little bit here to Dr. Horner's reference to the "protein binder" sex hormone-binding globulin- SHBG. Understanding this protein can make a big difference in your understanding of the "big picture" of hormone health and balance. It is a critical player with a big impact on all our hormones.

As Dr. Horner mentioned, estrogen (and other hormones) that are bound to SHBG are in the "carpool lane" and cannot make random exits from the bloodstream. Only "free" (unbound) estrogen can roam through various tissues of the body searching for estrogen receptor sites to lock on to. In terms of our risk for breast cancer, it is only the free estrogen that concerns us. However, there is more to the story.

The inner intelligence of the body doesn't want hormones running wild or falling below a certain level. It wants normalcy, hormonal law and order. To achieve this, your body utilizes these sex hormone-binding globulins, which are produced by the liver.

These proteins chaperone individual hormone molecules though the blood. Should the hormones reach too high a level, the protein binds and inactivates them – sort of like a handcuffing effect. The protein not only transports but also regulates and assists in the access process at target cell sites.

If the estrogen level goes too high, an alarm goes off in the liver, the body's master chemical factory. It pumps out extra SHBG. In reaction to a high tide of estrogen, your liver can produce up to three times the normal amount of SHBG.

The problem is that this special protein doesn't just bind up some of the excess estrogen. It binds up – and inactivates – some of the other important hormones, such as thyroid hormone, growth hormone and testosterone (which is more important for women than you might think!)

You may have heard of a condition referred to as "Estrogen Dominance". This is where the body is flooded with higher than necessary levels of estrogens, which might be produced by your own body, or come from a toxic source, xenoestrogens. Usually it is a combination of both.

In addition to the deleterious effects we have already discussed in regards to excess estrogen in the body, there is now a complicating factor. High levels of estrogen in the body trigger the release of sex hormone-binding globulin, as the body tries to maintain balance by inactivating some of the excess estrogen. But, at the same time the estrogen is being inactivated, the release of high amounts of SHBG causes other important hormones to become bound and inactive as well.

In this way estrogen dominance not only raises our risk for breast cancer, but can cause a cascade effect on other important hormones as well.

The effect on you is not immediate. It takes about six weeks before you usually start to experience the fallout from the lowered hormonal activity. Quantities of your important anti-aging hormones have now been taken out of commission. In essence, the available amount of these hormones falls to levels you might have when you are years older. The body becomes less "alive". Perhaps the skin becomes less radiant, the vagina drier. Lowered thyroid, for instance, can cause weight gain, fatigue, coldness and dry skin. These are all signs of a thyroid deficiency. Elevated SHBG can cause such multiple effects.


♦NBE Formula→Free Testosterone→5 alpha inhibitors→Aromatase→E1/E2....DNA→RNA→Protein ♦
♦Regulation of Estrogen & Progesterone-Hypothalamus→GnRH→Pituitary→FSH→Follicle→Estrogens ♦
♦ego cogito, ergo sum TG.
 Reply

 


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