[Koko]

Thanks, lotus! Amazing.

[ellacraig]

The most potent was y-Linolenic acid, GLA-aka EPO-Evening Primrose Oil.

Maybe thats the reason why I did grow last year when I took EPO. I definitely will up my dose to two capsules now. Thanks Lotus.

I'm taking two too! Only for a couple weeks though

These oils target breast growth, madacamia, vitex, red clover targets ER-a (the growth receptor). The links provided are for fyi.

Coconut oil
http://www.amazon.com/Barleans-Organic-Virgin-Coconut-16-Ounce/dp/B002VLZ8D0/ref=sr_1_10?ie=UTF8&qid=1425050271&sr=8-10&keywords=coconut+oil

Cucumber oil
http://www.amazon.com/CUCUMBER-Undiluted-Pressed-Botanical-Beauty/dp/B00BX3RLD2/ref=sr_1_2?ie=UTF8&qid=1425049927&sr=8-2&keywords=cucumber+oil

Macadamia oil
http://www.amazon.com/Macadamia-Nut-Cold-Pressed-Liquid/dp/B0017OAHPQ/ref=pd_sbs_bt_1?ie=UTF8&refRID=0BAN3M7J6KP6K6V5CNMS

Nutmeg oil
http://www.amazon.com/Nutmeg-Essential-U...B005Y4CV72

Turmeric oil
http://www.amazon.com/Turmeric-100-Therapeutic-Grade-Essential/dp/B005CIK5U0/ref=pd_sim_bt_5?ie=UTF8&refRID=07KHAMV92SQF7DQVSZG5

Vitex extract
http://www.amazon.com/Natures-Answer-Alcohol-Free-Vitex-1-Fluid/dp/B00014F9YC/ref=sr_1_6/177-7490590-4453118?ie=UTF8&qid=1425065984&sr=8-6&keywords=chasteberry

Red clover oil
http://www.amazon.com/Natures-Answer-Alcohol-Free-Flowering-1-Fluid/dp/B0001VUXKU/ref=sr_1_3?s=hpc&ie=UTF8&qid=1425066423&sr=1-3&keywords=Red+clover+extract

L how would you use the vitex?

Of all the fats wouldn't coconut oil be the richest? Stupid coconut oil doesn't work for me topically. Tell you what though, im loving it in my coffee! It masks the alternative milk quite well

[Lotus]

Coconut oil makes connective tissue stronger, it's also anti-DHT. Lauric acid & Capric acid in coconut oil increases adipose (fat stores), turns into breast tissue. Ingesting coconut oil works too, maybe better.

I'd apply vitex directly to the breasts prior to adding any other oils, or add it to a drink.

Thanks Koko.

[Lotus]

I want to link these posts together, hopefully you'll see the importance of how fatty acids can and does have a huge impact on NBE. And considering how effective FA's are in low concentrations it's particularly appealing.


Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Human or rat microsomal 5 alpha-reductase activity, as measured by enzymic conversion of testosterone into 5 alpha-dihydrotestosterone or by binding of a competitive inhibitor, [3H]17 beta-NN-diethulcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one ([3H]4-MA) to the reductase, is inhibited by low concentrations (less than 10 microM) of certain polyunsaturated fatty acids. The relative inhibitory potencies of unsaturated fatty acids are, in decreasing order: gamma-linolenic acid greater than cis-4,7,10,13,16,19-docosahexaenoic acid = cis-6,9,12,15-octatetraenoic acid = arachidonic acid = alpha-linolenic acid greater than linoleic acid greater than palmitoleic acid greater than oleic acid greater than myristoleic acid. Other unsaturated fatty acids such as undecylenic acid, erucic acid and nervonic acid, are inactive. The methyl esters and alcohol analogues of these compounds, glycerols, phospholipids, saturated fatty acids, retinoids and carotenes were inactive even at 0.2 mM. The results of the binding assay and the enzymic assay correlated well except for elaidic acid and linolelaidic acid, the trans isomers of oleic acid and linoleic acid respectively, which were much less active than their cis isomers in the binding assay but were as potent in the enzymic assay. gamma-Linolenic acid had no effect on the activities of two other rat liver microsomal enzymes: NADH:menadione reductase and glucuronosyl transferase. gamma-Linolenic acid, the most potent inhibitor tested, decreased the Vmax. and increased Km values of substrates, NADPH and testosterone, and promoted dissociation of [3H]4-MA from the microsomal reductase. gamma-Linolenic acid, but not the corresponding saturated fatty acid (stearic acid), inhibited the 5 alpha-reductase activity, but not the 17 beta-dehydrogenase activity, of human prostate cancer cells in culture. These results suggest that unsaturated fatty acids may play an important role in regulating androgen action in target cells.

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.
http://www.ncbi.nlm.nih.gov/pubmed/1637346

GLA- gamma-Linolenic acid (like EPO evening primrose oil),

gamma-Linolenic acid does not inhibit 17 beta HSD dehydrogenase activity, which one has yet to be identified


Btw, 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) play an important role in the regulation of steroid hormones, such as estrogens and androgens.

http://www.ncbi.nlm.nih.gov/pubmed/12570693

It was only a matter of time when this info would be found, enjoy.

Inhibition of steroid 5a-reductase by specific aliphatic unsaturated/fattyacid
http://www.ncbi.nlm.nih.gov/pmc/articles...1-0210.pdf

fatty acids could function as endogenous inhibitors of 5a-reductase


The most potent was y-Linolenic acid, GLA-aka EPO-Evening Primrose Oil.

From the first study,

Type 1 & 5 (17beta HSD) are breast growth potentiators

[Lotus]

This post follows up the previous information. Btw, the PDF is a complete version of the study.

Remember these "on and off" switches?, part of this good news, the other part.....not so good.

----------------------

The good news....…

the reductase responsible for the conversion of estrone (a weak estrogen) to 17b-estradiol (a potent estrogen) is the estrogenic type 1 17b-HSD and is the `on' switch for the estrogen receptor (ER). The oxidase activities responsible for the reverse reaction and the inactivation of 17b-estradiol are the type 2 and type 4 17b-HSDs, and these function as the `off' switch for the ER.

Thus, the activity of these 17b-HSD isoforms may regulate the ligand occupancy of ERa and ERb and their trans- activation in estrogen target tissues (Wu et al., 1993; Andersson, 1995; Labrie et al., 1997; 2000).

Hydroxysteroid dehydrogenases and pre-receptor regulation of steroid hormone action http://humupd.oxfordjournals.org/content...3.full.pdf

---------------------------------

The not so good news.....

Phytoestrogens inhibit human 17b-hydroxysteroid dehydrogenase type 5
http://www.brc.dcs.gla.ac.uk/~rb106x/pub...bition.pdf

This is a bit over simplified but Hydroxysteroid Dehydrogenases (HSDs) act like a gate-keeper just before steroids (hormones) bind to receptors (synthesis). Furthermore, these "gate-keepers" can flip the switch (a light switch) on/off to allow passage to the cell receptors. So in essence, they can inhibit or promote hormone activity. Finding a new class of HSD's is the next step, Aldo-keto reductases (AKRs) can help us get there.

[spanky (aka Lola)]

The not so good news.....

Phytoestrogens inhibit human 17b-hydroxysteroid dehydrogenase type 5
http://www.brc.dcs.gla.ac.uk/~rb106x/pub...bition.pdf

That is, as they say, a real kick in the (shrinking) nuts! A "potent inhibitor" of aromatase no less! So something like PM is a direct provider of a phytoestrogen to boost breast growth, but also it defeats aromatase conversion, thus undermining breast growth from the other direction! I have been combining PM with WP for a few months, and may have been largely wasting the WP! AARRGGHH! (No, I am not a pirate.)

If that analysis is correct, then is it an either/or situation, in which you must choose your weapon but not combine them?

[The First Aria]

Not so sure Spanky. I have been using WP and PM together for about 45 days, I think. My breast feel much fuller and when measured, by tape, it looks like I have jumped at least 1/4 inch in the last 3 weeks.

I think, IMO, that in your mind, PM stops ALL aromatase conversion. It might, if your testicles have all but shut down. Even if you are on the low end, whatever T is free might be converted. At least it seems in my case. My new Doctor ordered almost a full hormone panel and my T is about mid range. I have been using PM since last October and my test was just done a month ago. I think maybe if I were on PM for another 3-5 months my T would be somewhat lower, but not sure. As long as I have that much Total T floating around, I will utilize everything I have, in regards to aromatase.

[spanky (aka Lola)]

Not so sure Spanky. I have been using WP and PM together for about 45 days, I think. My breast feel much fuller and when measured, by tape, it looks like I have jumped at least 1/4 inch in the last 3 weeks.

I think, IMO, that in your mind, PM stops ALL aromatase conversion. It might, if your testicles have all but shut down. Even if you are on the low end, whatever T is free might be converted. At least it seems in my case. My new Doctor ordered almost a full hormone panel and my T is about mid range. I have been using PM since last October and my test was just done a month ago. I think maybe if I were on PM for another 3-5 months my T would be somewhat lower, but not sure. As long as I have that much Total T floating around, I will utilize everything I have, in regards to aromatase.

I hope you are right, that the aromatase inhibition is a minor effect. Until I am convinced there is a good alternative to phytoestrogens like PM, I will probably stick with the combination too. Also, I have no idea how much unsaturated fatty acid one would have to consume to match the breast growth potential of PM.

I have two important goals, prevention of prostate cancer and breast growth. WP seems to be helpful on both fronts, so I would hate to drop it. The same may be true for PM, although I do not know how it affects prostate cancer risk.

[spanky (aka Lola)]

Not so sure Spanky. I have been using WP and PM together for about 45 days, I think. My breast feel much fuller and when measured, by tape, it looks like I have jumped at least 1/4 inch in the last 3 weeks.

I think, IMO, that in your mind, PM stops ALL aromatase conversion. It might, if your testicles have all but shut down. Even if you are on the low end, whatever T is free might be converted. At least it seems in my case. My new Doctor ordered almost a full hormone panel and my T is about mid range. I have been using PM since last October and my test was just done a month ago. I think maybe if I were on PM for another 3-5 months my T would be somewhat lower, but not sure. As long as I have that much Total T floating around, I will utilize everything I have, in regards to aromatase.

[Lotus]

The health benefits of phyto's are well documented (especially here). These intracellular pathways are very interesting to say the least. That fact that someone did these kinds of studies blows me away lol. The estrogen receptor bioavailability chart I listed on another thread ties into these two studies. Put them all together and you get the sense of a reality check of sorts on NBE. The takeaway is that this info explains why we have slow, or no growth at all for some. Plus, I would even go as far to say the same holds true for HRT, and that glaring fact was E2 wasn't strong at binding to ER-a (the growth receptor). Which explains why HRT is slow going too, which if I did HRT I'd add these things below, that's just my opinion though. Estradiol (E2) doesn't all get bound to the estrogen receptors. Consider this though, increased levels of phyto's block out the body's own "natural estrogens", I'd say that's something you can ill afford when trying to grow breasts.



I think the obvious choice is to balance herbs that are PRO-ER-a with ER-b (protective receptor). Turmeric, green tea, essential fatty acids, and certain phtyoestrogens. 5 ar inhibitors are still a viable choice, reishi binds to ER's, not sure which one yet. WP is still a good choice. New weapons are things like 17 beta HSD's, type 1 & 4, plus CYP19 is still a viable option considering the andro to estro pathway,(that backdoor pathway is yet to be tapped).


cAMP or cyclic adenosine monophosphate is another possible NBE tool. Imo cAMP ties into fatty acids, or in large part how cAMP delivers FA's to hormones. In other words increasing blood flow to the receptors increase their bioavailability. Forilskin comes to mind, but quite honestly I think fatty acids work quite the same way.

cAMP is a second messenger important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.

cAMP is a second messenger, used for intracellular signal transduction, such as transferring the effects of hormones like glucagon and adrenaline, which cannot get through the cell membrane. Its purposes include the activation of protein kinases and regulating the effects of adrenaline and glucagon. It is also used to regulate the passage of Ca2+ through ion channels.

cyclic adenosine monophosphate
http://psychology.wikia.com/wiki/Cyclic_...ophosphate

-----------------------------

Bottom line- low dose esstential fatty acids (eg-EPO) 2000 mg and 2000 mg omega 3's, coconut oil 2000 mg will have a big effect on ER-a bioavailability over straight use of phytoestrogens. And for more depth, RC, Vitex, Hops all have an ER-alpha affinity. Balance with turmeric, green tea, progesterone, WP, reishi and boobie friendly foods that's been shared and its a solid program.

Massage, yoga, walking, hydration, etc are needed too. Remember, not everyone carries the same growth genes (DNA) for breast growth, meaning some are more sensitive to ER-a's over others. But!!!!, you absolutely "DO NOT" want to put yourself at risk with crazy herb dosages. If you've spent all this time and money on growing those boobs then why wouldn't you want an insurance policy ( eg-protective measures against breast cancer[tumeric,green tea]) which can even happen with
phytoestrogens, (always proceed with caution).

Research research, get all the facts, weigh all the options and then make an informed decision on an NBE program. 95% of that info is already here in the NBE archives, yup!, you gotta read it. And as always check with your primary care Doc.