My observation FWIF (unscientific) for optimal serum hormone levels goes like this:

NBE
E2 150-200 pg/ML
Total T 100-200 ng/dL (below this and libidos tank)
SHBG 66 nnmol/L

HRT
E2 400-800 (emulates menstrual cycles)
Total T 25 and below ng/dL (chemical castration)
SHBG 80 nnmol/L

Deny DHT's pathway (as much as possible) at the top of the chain (P450 family of enzymes) seems viable. Classic and side/backdoor leakage of DHT means we're chasing a fathom ghost inhibiting it. And it's time to go ghost hunting lol.


Metabolism of Testosterone, Dihydrotestosterone, Estrone and Estradiol
http://www.ergogenics.org/anabolenboek/index11en.html
The biosynthesis of the sex hormones starts with the oxidation of the side chain of cholesterol, which is catalyzed by the enzyme cytochrome P450scc. This cytochrome P450 oxidizes the side chain on C20 and C22 by the introduction of two hydroxyl groups. After that the chain is broken in between these two atoms by the same enzyme, under formation of pregnenolone.

The next steps in the biosynthesis of testosterone can proceed via two different routes. Pregnenolone can be oxidised first by cytochrome P45017a to 17a-hydroxypregnenolone. This route is known as the 5-ene route because all biosynthetic intermediates in this route possess a D5-double bond.

The enzyme 3b-HSD also can convert pregnenolone first into progesterone by oxidation of the 3b-hydroxy group followed by a shift of the double bond from the C5-C6 to the C4-C5 position. This route is known as the 4-ene route because here all biosynthetic intermediates possess a D4-double bond.

The reduction of testosterone takes place in target tissues like the prostate and the skin and of course metabolism takes place in the liver. In male a very small part (0.2%) of the testosterone is converted into estradiol. This process mainly takes place in adipose tissue and for about 20% in the testes.

The metabolisme of testosterone and dihydrotestosterone takes place for 90% in the liver. There reductases and dehydrogenases catalyse the reactions of the D4-double bond, the C3-carbonyl group and the C17-hydroxyl group. Finally the hydroxyl groups are connected to glucuronic acid or sulphate, followed by excretion with the urine [3] [4].


The biosynthesis of the female sex hormones starts from A-dione and can proceed by two different routes (see Scheme 2). The C17 carbonyl group in A-dione can be reduced first to a 17b-hydroxyl group under formation of testosterone, followed by oxidation and removal of the C19 methyl group and aromatisation of ring A.

The oxidation and removal of the C19 methyl group and the aromatisation of ring A can take place also first, under formation of estrone. Reduction of the carbonyl group at C17 then gives estradiol.

The oxidation of the C19 methyl group is catalyzed by a complex of cytochrome P450 enzymes, indicated with the code P450aromatase or simply as aromatase. The methyl group is first oxidized to a hydroxyl group and than to a carbonyl group (an aldehyde). The removal of this group together with a H-atom from C1 than leads to aromatisation of ring A. An important step in this aromatisation process is the fission of the C10-C19 bond. Also this reaction proceeds in only one direction. In chapter 15 more will be explained about aromatisation of anabolic steroids.

Within 15 minutes of any NBE/HRT supplementing, massage, pumping should be followed by some form of exercise that illicits a release of hormonal synthesis between (supplementations mentioned) and metabolized release of energy.

So the hypothalamus has been holding out on us, it turns out it controls appetite too, that sneaky thing.

Obesity results from an imbalance between energy intake and energy expenditure. The brain is an integral regulator of energy intake and energy expenditure, and thus whole-body energy homeostasis. The hypothalamus is important to the central regulation of energy homeostasis in the hypothalamic ARC control of food intake and regulation of energy balance, the mechanism(s) by which this occurs has not been established. Malonyl CoA inhibits carnitine palmitoyltransferase-1 (CPT-1), and it has been proposed that the substrate of CPT-1, long-chain acyl CoA(s), may act as a mediator(s) of appetite and energy balance.
Targeting Intermediary Metabolism in the Hypothalamus as a Mechanism to Regulate Appetite
http://pharmrev.aspetjournals.org/content/62/2/237.full.pdf

In particular, inhibiting FAS (fatty acids synthase) suppresses appetite via an increase malonyl CoA, exactly where do we find malonyl CoA???.......it's in leptin (or shall we say the release of leptin).

Leptin, an anorexigenic hormone secreted from adipocytes, can increase malonyl CoA levels in the ARC by activating ACC (Gao et al., 2007b). Recent evidence suggests that this up-regulation of malonyl CoA in the ARC mediates the anorectic signaling actions of leptin (Gao et al., 2007b

The inhibition of FAS has been attributed to an increase of malonyl CoA levels in the hypothalamus (Hu et al., 2003), which subsequently is linked to an increase of fatty acid oxidation rates in skeletal muscle (Cha et al., 2005, 2006)

Hypothalamic malonyl-CoA and the control of food intake.
Gao S, et al. Physiol Behav. 2013.

Abstract
Fatty acid metabolism is implicated in the hypothalamic control of food intake. In this regard, malonyl-CoA, an intermediate in fatty acid synthesis, is emerging as a key player. Malonyl-CoA in the hypothalamus has been proposed as an anorectic mediator in the central control of feeding. A large body of evidence demonstrates that modulating hypothalamic activities of malonyl-CoA metabolic enzymes impacts food intake. Malonyl-CoA action appears to play a significant role in the intracellular signaling pathways underlying leptin anorectic effect in the arcuate nucleus. Ghrelin's hypothalamic effect on feeding may also involve the change in malonyl-CoA metabolism. Hypothalamic malonyl-CoA levels are altered in response to fasting and refeeding, suggesting physiological relevance of the changes in malonyl-CoA level in the controls of feeding and energy balance. -CoA inhibits the acyltransferase activity of carnitine palmitoyltransferase-1 (CPT-1), and CPT-1 was considered as a downstream effector in hypothalamic malonyl-CoA effect on feeding. However, recent evidence has not been entirely consistent with this notion. In the arcuate nucleus, the inhibition of CPT-1 acyltransferase activity does not play an important role in the feeding effect of either leptin or cerulenin (a fatty acid synthase inhibitor) that requires the increase in malonyl-CoA level. Alternatively, the brain isoform of CPT-1 (CPT-1c) may act as a downstream target in the malonyl-CoA signaling pathways. CPT-1c does not possess a typical acyltransferase activity, and the exact molecular function of this protein is currently unknown. Recent data indicate it is involved in ceramide metabolism. Of relevance, in the arcuate nucleus, CPT-1c may link malonyl-CoA to ceramide metabolism to affect food intake.

© 2013. PMID 23988346 [PubMed - indexed for MEDLINE] PMCID PMC4803278


So.......what does this mean for NBE?, imo.....the release of leptin can inhibit appetite and oh btw release aromatase. Say what!!!!

the hypothalamus contains several contains several clusters of neurons, commonly designated as nuclei. Current research indicates that one of these, the arcuate nucleus, houses the appetite center.

Appetite, Metabolism and Obesity
http://www.medbio.info/Horn/PDF%20files/Appetite%20and%20weight%20control%20January%202013a.pdf

Very interesting article Lotus. Thanks, POM

Very interesting article Lotus. Thanks, POM

Thanks POM, I'm intrigued by this news, controlling appetite can help obesity for sure. An empty stomach triggers (or initiates) the hormone ghrelin " the hunger hormone ".

The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review.
http://www.ncbi.nlm.nih.gov/m/pubmed/17212793/

I wonder if scientists have figured out a ratio of leptin over ghrelin in controlling hunger??, for another day perhaps (calling it a night lol).

Very interesting article Lotus. Thanks, POM

Thanks POM, I'm intrigued by this news, controlling appetite can help obesity for sure. An empty stomach triggers (or initiates) the hormone ghrelin " the hunger hormone ".

The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review.
http://www.ncbi.nlm.nih.gov/m/pubmed/17212793/

I wonder if scientists have figured out a ratio of leptin over ghrelin in controlling hunger??, for another day perhaps (calling it a night lol).

-----------------------------------------
Good Night, and Sweet Dreams.

Thanks POM.

I have some additional info relating to cold water/ice therapy talked about in previous post (below) specifically called Cold thermogenesis, CT for short. I think we step up CT by adding another option.........iced pumping, (noogling?, you get the picture). I also do a variation of taking ice packs directly over the breast while doing a cycle of isometrics (i.e, arms folded accross chest and flex each breast [separately] to the point of muscle fatigue).

The idea is to create new BAT (brown adipose tissue) by thermogenesis. Only in my opinion (lol) as we expend burned energy (via thermogenesis) fat is oxidized through mitochondria through HSP (heat shock proteins), some evidence has shown that when HSP's are increased it protects against oxidative stress, (this is postive news imo, similar to anti-inflammatories, only here, it's produced naturally in our cells). Now when I do this CT my heart rate immediately goes up, which activates this process too. Please seek medical advice before beginning any NBE regiment. I'm not a medical professional.

Combining cold thermogenesis with HIIT (high intensity interval training) aka depletion of energy in breast tissue could be of benefit. Add intermittent fasting to kick HGH (human growth hormone) in.

when you consume protein in levels higher than recommended above, you tend to activate the mTOR (mammalian target of rapamycin) pathway, which can help you get large muscles but may also increase your risk of cancer. There is also research suggesting that the "mTOR gene" is a significant regulator of the aging process, and suppressing this gene may be linked to longer life.

http://fitness.mercola.com/sites/fitness/archive/2014/09/26/intermittent-fasting-hiit-workout.aspx#!

Anyways lol. I'm getting ahead of myself lol, I'll have to break other related info over a couple of posts. Though some keys points are icing breasts while doing isometrics, try a cold version of pumping (crushed ice insides the domes), and do isometrics while pumping for fat burn.

The best part of this cold therapy (cold thermogenesis) is the low cost of ice water lol . And there's plenty of diy versions of ice packs.


Another version of thermogenesis happens when we sleep, natural melatonin plays a part of this. Adding melatonin at night (because we lose the natural production over time) with MSM looks very interesting, more info to follow:

Proof of principle: the effects of chemical uncouplers:
The mitochondria of any organ of the body (except brown adipose tissue) are innately energy sparing through the ‘coupling’ of O2 consumption (i.e. thermogenesis) to ATP synthesis, only allowing the combustion of substrate when it is necessary, i.e. when ADP is available to be phos- phorylated (Fig. 2(A)). As heat is released when ATP is hydrolysed, thermogenesis can in principle occur either when ATP utilization is increased (e.g. in muscular work) or when protons are allowed to re-enter the mitochondria without ATP synthesis taking place, i.e. in ‘uncoupled’ mitochondria (Fig. 2(B and C)).
http://journals.cambridge.org/download.php?file=%2FPNS%2FPNS68_04%2FS0029665109990255a.pdf&code=ae00444e6022919fff41ae708a1ef5e1#xml=http://journals.cambridge.org/data/userPdf/

Functional Brown Adipose Tissue in Healthy Adults
studies in healthy subjects show that cold-induced glucose uptake in supraclavicular adipose-tissue depots is increased by a factor of 15 and that this tissue expresses mRNA for markers of brown adipose tissue
http://www.nejm.org/doi/full/10.1056/NEJMoa0808949#discussion

Hi BN,


So I was looking into some research on cold water therapy and how it aids in recovery times in post HIIT workouts. Turns out that it also builds new brown fat cells, hmm, interesting huh?. Well.....it got me thinking on different ways to promote new cell growth for breast tissue. As we know fat cells produce aromatase enzyme, which converts testosterone into estrogen. We also know HIIT produces natural growth hormone and lactate, (initiates new muscle synthesis). It's quite possible (imo) using that cold water therapy and HIIT can trigger breast growth, the science says it's possible.

Another example: From a clinical study I found that it stated that cAMP (2nd messengers) levels significantly increased lipolysis in adipose tissue, at 4°C, (39 degrees). Adipocytes increased the release of glycerol, indicating that the high rate of lipolysis occurred in these cells.


So how do this apply to NBE?, my opinion?..........hmm....... use ice packs on the boobs after massage/boobie exercises (you still do those grab n pull method boob exercises right?) I hope so cause that in-itself triggers breast growth. This method along with HIIT, cold water therapy is free, cept the cost of water.

Initiation of myoblast/brown fat switch through a PRDM16-C/ EBP-β transcriptional complex:

These data indicate that the PRDM16-C/EBP-β complex initiates brown fat development from myoblastic precursors, and may provide opportunities for the development of novel therapeutics for obesity and type-2 diabetes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754867/pdf/nihms132247.pdf

EFFECT OF IMMEDIATE AND DELAYED COLD WATER IMMERSION AFTER A HIGH INTENSITY EXERCISE SESSION ON SUBSEQUENT RUN PERFORMANCE
http://www.jssm.org/vol10/n4/10/v10n4-10text.php

In summary, quantitative and qualitative analyses demonstrated that immediate CWI performed after a HIIS resulted in better next day running performance (YRT), while delayed (3 h) CWI was also likely to result in improved YRT performance, compared to no CWI. Importantly, greater benefit was associated with immediate CWI. This information is pertinent to athletes, particularly if they do not have immediate access to recovery facilities following exercise performance.

______________________________________________

The 16 Secret Benefits of Taking a COLD SHOWER
http://www.naturalmuscle.net/#!The-16-Secret-Benefits-of-Taking-a-COLD-SHOWER/cn2j/5508937a0cf2031a764c7ad6

Thanks Lotus,
Its scary.. I think I'm beginning to understand some of this stuff.
Bobbi
Are you going to continue expanding this thread?

Haha that is scary cool Boobi, this stuff drives you to new ideas and understanding for sure. For instance, this idea of what free energy does in metabolism makes thermogenesis so interesting, and specifically how we use adipose (fat tissue) to promote the body's own release of E2. The study below suggests we're not too far from pressing play without great difficulty (aka• aromatase to E2). I'll probably fold in the other research threads I have to the program x thread, it makes it easy to reference material in one section.


Non-exercise activity thermogenesis.
Review article
Levine JA. Proc Nutr Soc. 2003.
Show full citation
Abstract
Non-exercise activity thermogenesis (NEAT) is the energy expended that is not from sleeping, eating or sports-like exercise. It ranges from the energy expended walking to work, typing, performing yard work, undertaking agricultural tasks and fidgeting. NEAT can be measured by one of two approaches. The first approach is to measure or estimate total NEAT. Here, total daily energy expenditure is measured and from it is subtracted BMR + thermic effect of food. The second is the factoral approach whereby the components of NEAT are quantified and total NEAT calculated by summing these components. The amount of NEAT that human subjects perform represents the product of the amount and types of physical activities and the thermogenic cost of each activity. The factors that affect the NEAT of a human subject are readily divisible into biological factors, such as weight, gender and body composition, and environmental factors, such as occupation or dwelling within a 'concrete jungle'. The combined impact of these factors explains the substantial variance in human NEAT. The variability in NEAT might be viewed as random but human data contradict this perception. It appears that changes in NEAT subtly accompany experimentally-induced changes in energy balance and are important in the physiology of weight change. NEAT and sedentariness may thus be important in obesity. It then becomes intriguing to dissect mechanistic studies that delineate how NEAT is regulated by neural, peripheral and humoral factors. NEAT may be a carefully-regulated 'tank' of physical activity that is crucial for weight control.

PMID 14692603 [PubMed - indexed for MEDLINE]

The repost is worth another look: the link (awesome) below has helped us understand how T, SHBG, free T, albumin works.

Cholesterol is the precursor (for all hormones) that converts testosterone (via the leydig cells,) which sigals the lutenizing hormone ------to either produce more or less T, other factors regulate this process too though. These formulated esters can be tanking NBE imo and we don't even know yet. (Yikes)

For the non geek types it might be easier to see T explained from this publication:

how testosterone is made
http://www.artofmanliness.com/2013/01/15/how-testosterone-is-made/

Note: referenced under " where and how testosterone is made " no. 4

Ideas towards feminization,

• Liver activation of protein/enzymes & hormones
  
• Growth Hormone signal via CYP2AB enzyme
  
• Increased GH (growth hormone) secretion via the hypothalamus
  
• Inhibit lutenizing hormone
  

NBE key tools

• 
  Foods
  
• Lemons, oranges, red pigment fruits and veggies.....all of which inhibits CYP17 enzyme (a key enzyme in the steroid biosynthesis of androgens)
  
• Green tea-also a CYP17 inhibitor / also a CYP19 promoter (aka-aromatase)
  
• walnuts (1/4 cup) 2-3x a week, pro ER-a, antioxidant, w-6 fatty acid
  
• Drink (min) 4 cups of green tea daily (80-98% polyphenols)
  
• Drink filtered water 6-8 cups (add a slice of fresh lemon)
  
• Get 10 minutes of high intensity work outs 3-4x a week
  
• Reduce coffee (1 cup per day)
  
• Add protein and healthly fats
  
  _____________________________
  
  Supplements
  
• White peony extract (2-3 per day) pro-aromatase, 5 alpha reductase inhibitor (inhibits DHT).
  
• Red clover extract (1-2 per day)......,low progesterone effect, pro-estrogen alpha receptor promoter. pro-areolas
  
• Authentic PM 1000mg (total).....up to 250 mg for women, days 1-14 (after periods ends)........pro-estrogen mimic, activates CYP2AB enzyme (necessary for feminization)
  
  
• Progesterone cream (applied to breasts, 3-4 times per week).....progesterone
  
• L-arginine (1 per day)........amino-acid, for activation of growth hormones signaling.
  
• reishi 1-2 (per day)........anti-androgen
  
• astaxanthin (1-2 per day)......anti-androgen
  
• niacin (inositol) 1-2 per day
  
• MSM, antioxidant, pro-breast health, GH (growth hormone) STAT5 protein synthesizer.......
  
  

Green Tea - stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream. why is this important?, 95-98% fatty acids are bound in the blood stream (just like hormones are), we needed something that displaces hormones and fatty acids, looks like green tea is up for the task.


The Potential of Citrus Limonoids as Anticancer Agents
http://ucce.ucdavis.edu/files/datastore/234-200.pdf

Ideas towards feminization,

• Liver activation of protein/enzymes & hormones
  
• Growth Hormone signal via CYP2AB enzyme
  
• Increased GH (growth hormone) secretion via the hypothalamus
  
• Inhibit lutenizing hormone
  

NBE key tools

• 
  Foods
  
• Lemons, oranges, red pigment fruits and veggies.....all of which inhibits CYP17 enzyme (a key enzyme in the steroid biosynthesis of androgens)
  
• Green tea-also a CYP17 inhibitor / also a CYP19 promoter (aka-aromatase)
  
• walnuts (1/4 cup) 2-3x a week, pro ER-a, antioxidant, w-6 fatty acid
  
• Drink (min) 4 cups of green tea daily (80-98% polyphenols)
  
• Drink filtered water 6-8 cups (add a slice of fresh lemon)
  
• Get 10 minutes of high intensity work outs 3-4x a week
  
• Reduce coffee (1 cup per day)
  
• Add protein and healthly fats
  
  _____________________________
  
  Supplements
  
• White peony extract (2-3 per day) pro-aromatase, 5 alpha reductase inhibitor (inhibits DHT).
  
• Red clover extract (1-2 per day)......,low progesterone effect, pro-estrogen alpha receptor promoter. pro-areolas
  
• Authentic PM 1000mg (total).....up to 250 mg for women, days 1-14 (after periods ends)........pro-estrogen mimic, activates CYP2AB enzyme (necessary for feminization)
  
  
• Progesterone cream (applied to breasts, 3-4 times per week).....progesterone
  
• L-arginine (1 per day)........amino-acid, for activation of growth hormones signaling.
  
• reishi 1-2 (per day)........anti-androgen
  
• astaxanthin (1-2 per day)......anti-androgen
  
• niacin (inositol) 1-2 per day (helps receptor synthesis)
  
• MSM, antioxidant, pro-breast health, GH (growth hormone) STAT5 protein synthesizer.......
  
  

Green Tea - stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream. why is this important?, 95-98% fatty acids are bound in the blood stream (just like hormones are), we needed something that displaces hormones and fatty acids, looks like green tea is up for the task.


The Potential of Citrus Limonoids as Anticancer Agents
http://ucce.ucdavis.edu/files/datastore/234-200.pdf

---------------------------------------------
Thanks for this Lotus, and I like your new avatar. POM