[wee2er]

I've been doing some re-reading through your (@Lotus) fantastic notes and came across aloe vera gel and olive oil.
Used in 50:50 quantities - apply olive oil first and let it sink in then apply the aloe vera gel.
Am I right in thinking that this combo could be used as a good alternative for prog cream (PC)?
If so, would the same combo work if applied to butt/thighs area to develop more curves down below? 

[Lotus]

Am I right in thinking that this combo could be used as a good alternative for prog cream (PC)?
If so, would the same combo work if applied to butt/thighs area to develop more curves down below? 

I think you'll still need progesterone to achieve more curves down below. 

Hi Weezer, I do remember that exact post, here's additional info on aloe below. How Olive Oil works with aloe is by helping it as a carrier oil. However, when I posted about the two used together I thought Olive oil worked more as Binding Protein (e.g. fatty-acid-binding proteins, FABPs)... or like PPAR’S (peroxisome proliferator-activated receptors, info below). Estradiol has low solubility in blood and needs a binding protein to carry them in the bloodstream... to bind in tissues (e.g. breasts). Oh and, apologies for the long post.

And here's where aloe vera comes in. Of the 75 compounds collagen is one of them, and I explain how it can be used for NBE.
Collagen is the major protein in the extracellular matrix (ECM) of various connective tissues. It was observed that aloe vera increases the collagen content of the granulation tissue as well as its degree of crosslinking [13]. Aloe vera stimulates fibroblasts for regeneration in a synovial model [17], and enhances tensile strength and collagen turnover in damaged tissues [61]. In another trial using topical application, aloe vera gel stimulated fibroblast activity and collagen proliferation [16].
Aloe Vera for Tissue Engineering Applications
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5371879/

The 500 Dalton rule for the skin penetration of chemical compounds and drugs
Authors
* Jan D. Bos, Marcus M. H. M. Meinardi
* First published: June 2000Full publication history
* DOI: 10.1034/j.1600-0625.2000.009003165.xView/save citation
* Cited by: 370 articles

Jan D. Bos, Department of Dermatology A0-235, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands
Tel.: +31 20 566 2587. Fax: +31 20 696 0076
e-mail: j.d.bos@amc.uva.nl
Abstract
Abstract: Human skin has unique properties of which functioning as a physicochemical barrier is one of the most apparent. The human integument is able to resist the penetration of many molecules. However, especially smaller molecules can surpass transcutaneously. They are able to go by the corneal layer, which is thought to form the main deterrent. We argue that the molecular weight (MW) of a compound must be under 500 Dalton to allow skin absorption. Larger molecules cannot pass the corneal layer. Arguments for this “500 Dalton rule” are; 1) virtually all common contact allergens are under 500 Dalton, larger molecules are not known as contact sensitizers. They cannot penetrate and thus cannot act as allergens in man; 2) the most commonly used pharmacological agents applied in topical dermatotherapy are all under 500 Dalton; 3) all known topical drugs used in transdermal drug-delivery systems are under 500 Dalton. In addition, clinical experience with topical agents such as cyclosporine, tacrolimus and ascomycins gives further arguments for the reality of the 500 Dalton rule. For pharmaceutical development purposes, it seems logical to restrict the development of new innovative compounds to a MW of under 500 Dalton, when topical dermatological therapy or percutaneous systemic therapy or vaccination is the objective.
http://onlinelibrary.wiley.com/doi/10.10...x/abstract

Molecular Weights: (g/mol)
Aloe Vera- 270.24
Palmitic- 270.46
Stearic - 298.52
Oleic - 282.46
Linoleic - 298.48
Almond oil - 106.12
Estradiol - 272.4
Soybean oil -292.2

Oleic acid: its effects on stratum corneum in relation to (trans)dermal drug delivery.
Francoeur ML1, Golden GM, Potts RO.
Author information
Abstract
Calorimetric studies with porcine stratum corneum (SC) have shown that the lipid phase transitions associated with the intercellular bilayers are markedly affected by treatment with oleic acid. Specifically, the transition temperatures ™ and cooperativity are reduced, whereas no effect was observed on the endotherm associated with keratin denaturation, suggesting that oleic acid primarily affects the SC lipids. The decrease in the lipid-associated Tm's was further correlated with the amount of oleic acid taken up by the SC. Parallel experiments with silastic implied that the uptake is dependent on the thermodynamic activity of oleic acid in the vehicle itself. The in vitro transport of Piroxicam across human and hairless mouse skin (HMS) was significantly enhanced by oleic acid, as a function of the extent of oleic acid uptake, with an attendant change in Tm. These results emphasize the role of SC lipids in percutaneous absorption. Transport also depended on the donor concentration of ionized drug suggesting that the enhanced transport mechanism cannot be accounted for solely on the principles of the classical pH-partition hypothesis. Accordingly, a model of skin permeability enhancement involving solid-fluid phase separation within the SC lipids is proposed for oleic acid, consistent with the existing phospholipid literature. In conjunction with the use of oleic acid as an enhancer, very soluble hydrophilic salts were recognized as key factors in attaining maximum delivery. Oleic acid uptake, lipid delta Tm, and enhanced drug flux were all found to correlate, exhibiting a bell-shaped curve as a function of the ethanol vehicle concentration. Therefore, uptake and/or DSC experiments are useful for formulating enhanced topical delivery systems.

 Hi BN, 
Red Clover is beneficial for NBE. If you don't know what PPAR (peroxisome proliferator-activated receptor), you should. (Info supplied below). 
red clover extract: a putative source for simultaneous treatment of menopausal disorders and the metabolic syndrome.
Mueller M1, Jungbauer A.
Author information
Abstract
OBJECTIVE:
Currently, red clover extract is used to treat menopausal disorders as an alternative to classic hormone therapy. Several human and animal studies have attributed hypolipidemic, hypoglycemic, or antiatherosclerotic effects to red clover extract or isoflavones. This study was designed to determine the peroxisome proliferator-activated receptor (PPAR) gamma activation by red clover extract.
DESIGN:
The PPARgamma binding affinities and the transactivation activities of red clover extracts, isoflavones, and their metabolites were analyzed. The presence of specific substances in the extracts was proved by high-performance liquid chromatography/electrospray ionization/mass spectrometry.
RESULTS:
The red clover extracts and the compounds genistein and biochanin A were potent PPARgamma ligands and activators. Several metabolites exerted higher binding affinities or transactivational activities than their precursor molecules. 6-Hydroxydaidzein exerted a more than 100-fold higher binding affinity than its precursor daidzein. The maximal transactivational activity of 6-hydroxydaidzein and 3'-hydroxygenistein exceeded even that of rosiglitazone, a known PPARgamma agonist. Equol and O-desmethylangolensin showed an approximately fivefold higher binding affinity and, in the case of O-desmethylangolensin, a fourfold higher PPARgamma agonistic activity than the precursor. The daily dose of Menoflavon forte, a widely used red clover extract for treatment of menopausal disorders, provides theoretically 15% to 30% of the daily recommended dose of rosiglitazone. Considering the more active metabolites formed, activity must be higher in vivo.

CONCLUSIONS:
This study shows that red clover extracts, the major compounds, and especially several main metabolites exert significant PPARgamma binding and transactivation activity. Red clover extract, which is currently used for treating menopausal disorders, could be simultaneously used for ameliorating the metabolic syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/18724264

peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
Schoonjans K1, Staels B, Auwerx J.
Author information
Abstract
The three types of peroxisome proliferator-activated receptors (PPAR), termed alpha, delta (or beta), and gamma, belong to the nuclear receptor superfamily. Although peroxisome proliferators, including fibrates and fatty acids, activate the transcriptional activity of these receptors, only prostaglandin J2 derivatives have been identified as natural ligands of the PPAR gamma subtype that also binds thiazolidinedione antidiabetic agents with high affinity. PPARs heterodimerize with retinoic X receptor (RXR) and alter the transcription of target genes after binding to response elements or PPREs, consisting of a direct repeat of the nuclear receptor hexameric DNA recognition motif (PuGGTCA) spaced by 1 nucleotide (DR-1). Upon activation by fatty acids (FAs) and drugs that affect lipid metabolism, PPARs control the expression of genes implicated in intra- and extracellular lipid metabolism, most notably those involved in peroxisomal beta-oxidation. PPARs partially mediate the inductive effects of fibrates and fatty acids on high density lipoprotein (HDL) cholesterol levels by regulating the transcription of the major HDL apolipoproteins, apoA-I and apoA-II. The hypotriglyceridemic action of fibrates and certain fatty acids also involves PPAR and is constituted of: 1) increased hydrolysis of plasma triglycerides due to induction of LPL and reduction of apoC-III expression; 2) stimulation of cellular fatty acid uptake and conversion to acyl-CoA derivatives due to increased expression of genes for fatty acid transport protein and acyl-CoA synthetase; 3) increased peroxisomal and mitochondrial beta-oxidation; and 4) decreased synthesis of fatty acids and triglycerides and decreased production of very low density lipoprotein (VLDL). Hence, both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL particles contribute to the hypolipidemic effect of fibrates and fatty acids. Finally, PPARs appear to be involved in differentiation processes because activation of PPAR gamma 2 triggers adipocyte differentiation and stimulates expression of several genes critical to adipogenesis. It is suggested that PPARs are key messengers responsible for the translation of nutritional and pharmacological stimuli into changes in gene expression and differentiation pathways.
PMID: 8725145 [PubMed - indexed for MEDLINE] Free full text

Increase In Visceral Fat During Menopause Linked With Testosterone
http://www.sciencedaily.com/releases/200...161144.htm
In middle-aged women, visceral fat, more commonly called belly fat, is known to be a significant risk factor for cardiovascular disease, but what causes visceral fat to accumulate?
The culprit is likely not age, as is commonly believed, but the change in hormone balance that occurs during the menopause transition, according to researchers at Rush University Medical Center.
"Of all the factors we analyzed that could possibly account for the increase in visceral fat during this period in a woman's lifetime, levels of active testosterone proved to be the one most closely linked with abdominal fat," said Imke Janssen, PhD, assistant professor of preventive medicine and the study's lead investigator.
The study, which has been published early online in the medical journal Obesity, included 359 women in menopausal transition, ages 42 to 60, about half black and half white. Fat in the abdominal cavity was measured with CT scans, a more precise measurement than waist size. Blood tests were used to assess levels of testosterone and estradiol (the main form of estrogen). Medical histories covered other health factors possibly linked with an increase in visceral fat.

___________________________________________

Screening of herbal extracts for activation of the human peroxisome proliferator-activated receptor
http://www.ncbi.nlm.nih.gov/pubmed/17152989
The peroxisome proliferator-activated receptors play a pivotal role in metazoan lipid and glucose homeostasis. Synthetic activators of PPARalpha (fibrates) and PPARgamma (glitazones) are therefore widely used for treatment of dislipidemia and diabetes, respectively. There is growing evidence for herbal compounds to influence nuclear receptor signalling e.g. the PPARs. We recently reported carnosic acid and carnosol, both being diterpenes found in the labiate herbs sage and rosemary, to be activators of PPARgamma. The subsequent screening of a variety of ethanolic extracts, obtained from traditionally used herbs, for PPAR activation, led to an exceptionally high hit rate. Among 52 extracts nearly the half significantly activated PPARgamma and 14 activated PPARalpha in addition, whereas three of them were pan-PPAR activators, which also activated PPARdelta. The most active extracts, for which a concentration dependent effect could be shown, were the extracts of Alisma plantago aquatica (ze xie/european waterplantain), Catharanthus roseus (madagascar periwinkle), Acorus calamus (sweet calamus), Euphorbia balsamifera (balsam spurge), Jatropha curcas (barbados nut), Origanum majorana (marjoram), Zea mays (corn silk), Capsicum frutescens (chilli) and Urtica dioica (stinging nettle). The results of the present study provide a possible rationale for the traditional use of many herbs as antidiabetics.

Glitazones for type 2 diabetes
http://www.nps.org.au/conditions/hormone...glitazones
____________________________________
Anti-diabetic medication
Drugs used in diabetes treat diabetes mellitus by lowering glucose levels in the blood. With the exceptions of insulin, exenatide, liraglutide and pramlintide, all are administered orally and are thus also called oral hypoglycemic agents or oral antihyperglycemic agents. There are different classes of anti-diabetic drugs, and their selection depends on the nature of the diabetes, age and situation of the person, as well as other factors.
Diabetes mellitus type 1 is a disease caused by the lack of insulin. Insulin must be used in Type I, which must be injected.
Diabetes mellitus type 2 is a disease of insulin resistance by cells. Type 2 diabetes mellitus is the most common type of diabetes. Treatments include (1) agents that increase the amount of insulin secreted by the pancreas, (2) agents that increase the sensitivity of target organs to insulin, and (3) agents that decrease the rate at which glucose is absorbed from the gastrointestinal tract.
Several groups of drugs, mostly given by mouth, are effective in Type II, often in combination. The therapeutic combination in Type II may include insulin, not necessarily because oral agents have failed completely, but in search of a desired combination of effects. The great advantage of injected insulin in Type II is that a well-educated patient can adjust the dose, or even take additional doses, when blood glucose levels are measured by the patient, usually with a simple meter, as needed by the measured amount of sugar in the blood.
http://wikipedia.org/wiki/Anti-diabetic_drug

Thanks for reading 

[wee2er]

It's a pleasure Lotus with a BIG thank you to you, you are a wonderous font of all boobie growth knowledge 

I've just started using Prog cream the SMNutrition, Progesto-Life that many have used. Again from deep within your font of knowledge, you have said to use it only 3 times a week and to change where you apply it to?

As such I will be using it 3xtimes a week and rotating it to hopefully achieve:

• Breasts - fill out the inner / upper quadrants
  
• Inner thighs - fill out thighs
  
• Butt - fill out butt
  
• Face - possible feminisation of and reduce wrinkles / just a decent night time moisturiser
  
• Scrotum - not sure what this will do other than quicker absorption
  

My B cups are big enough so only wanting the PC to fill them out a bit as my focus has now turned to lower half feminisation.

Do you  think this be a decent PC regime to achieve my goals, or do you think I will need pharma prog pills ?

[CM213]

What's the difference between these two creams. Looking at the description they are both 4 oz, 2000 of micronised usp.  Here is the links for both

Progesterone Cream for Women Bioidentical 2000mg | From Wild Yam, Dermatologist-Tested | For Menopause & Menstrual Support | Micronized USP, Fragrance-Free & Soy-Free Topical ProgestoLife, 96 Servings https://a.co/d/7RQPZYO

Progesterone Cream for Women | 2000mg USP Micronized Progesterone for Balance & Menstrual Support | 4oz Pump (~96 Servings) | Soy-Free, Gluten-Free, Dairy-Free, Phenoxyethanol-Free, Cruelty-Free https://a.co/d/4EkhLa9

And is one better or more beneficial than the other? Thanks.

I am not starting any nbe program soon. Taking time off of everything nbe and steroids, to allow my body to get back to a normal balance through the summer. Work on my health (all aspects) and get to a desired weight before I start any nbe that may cause me to gain weight. I am just trying to research and learn what are the best products that I can source for myself without a prescription.

I plan to allow my body to reset over the summer and if all goes well and I feel I still want to feminize (which Im sure I will since this voice in my head has been there as long as I can remember.) then I will start a nbe routine late summer/end of summer/ beginning of fall here in the United States that way I can go through all the colder seasons and not worry about people noticing anything till next spring summer. And then I will cross that bridge when I get to it. I'll prob just say I've abused steroids for over a decade and that now I screwed up my hormones so much I got gyno and I don't have the time or money for the surgery to remove it. Sounds legit enough lol. They don't need to know that I have a feminine voice in my head that's screaming to be let out and heard and given a chance to thrive.

[SensualTiffany]

Edit (4/2/24) Hi BN, updating the plan to reflect new additions. 

Continuing the research, there's a strategy in using vitamin D3 and calcium (and actual relatable science) together in the Lotus NBE program, along with MSM that's been thought out very carefully that I'll share asap. But this first, vitamin D3 actually increases IGF-1, so as we worry about not getting enough IGF-1 for breast growth you've been getting if you've followed my plan…or taking 5,000iu to 7,000iu of vitamin D3 per day. Which is perfectly safe limits to take within these amounts, period. 

Vitamin D increases circulating IGF1 in adults: potential implication for the treatment of GH deficiency
Pietro Ameri et al. Eur J Endocrinol. 2013
Abstract

Objectives: Previous studies suggested that vitamin D modulates circulating IGF1. We investigated this effect in adults and its clinical relevance in the management of GH deficiency (GHD).

Design and methods: IGF1 levels were prospectively measured before and after 12 weeks of treatment with oral vitamin D3 (5000 or 7000 IU/week) vs no intervention in 39 subjects 61.9±7.9 years old. The frequency of IGF1 values ≥50th age- and sex-specific percentile in relation to vitamin D status, as determined by the concentration of 25-hydroxyvitamin D (25(OH)D), was retrospectively assessed in 69 GHD patients (57.4±16.6 years) on stable hormone replacement and with 25(OH)D and IGF1 concurrently measured.

Results: Treatment with 5000 and 7000 IU vitamin D3/week significantly raised 25(OH)D by 12.7±8.4 and 13.1±6.5 ng/ml respectively (both P<0.001 vs baseline). In the 7000 IU group, IGF1 levels also significantly increased by 31.3±36.7 ng/ml (P=0.01). Neither 25(OH)D nor IGF1 significantly varied in controls. IGF1 was ≥50th percentile more frequently in GHD patients with 25(OH)D levels ≥15 than <15 ng/ml(65.9 vs 40.0%, P<0.05). Logistic regression with adjustment for recombinant human GH (rhGH) dose, vitamin D supplements, gender, use of thyroid hormones, corticosteroids or estrogen/testosterone, and season revealed a significant positive association between ≥15 ng/ml 25(OH)D and IGF 1 ≥50th percentile (OR 4.4, 95% CI 1.0-18.8, P<0.05). A significant negative correlation between 25(OH)D concentrations and rhGH dose was found after correcting for age and IGF1 (β -0.042, P<0.01), but not after further adjusting for sex, thyroid, adrenal or gonadal replacement, and season (β -0.037, P=0.06).

Conclusions: Vitamin D increases circulating IGF1 in adults. As a result, a better vitamin D status may ease the achievement of normal IGF1 values in GHD.

Vitamin D regulates IGF1 concentrations in the liver, the main source of circulating IGF1

Pueraria mirifica @ 500-1500pm (daily) estrogenic, acts more like E1 (estrone) that initiates breast buds).
Progesterone cream- 1/4 teaspoon per breast (3-4 times per week, and only use after you've developed breast buds). If using prescription progesterone pills the dosage ranges between 100mg to 300mg. If I'm using progesterone as a topical application I'd only recommend 1 progesterone taken either orally or rectally. 
MSM 1-3g per day. antioxidant, taking msm facilitates a pro-breast growth pathway called STAT5, it's a protein synthesizer, Meaning it helps raise growth hormone.
Vitamin D3 & Calcium, helps with breast growing. If you take Calcium you need V-D3 to become more biologically active. Source vitamin D3 with organic olive oil. 
Melatonin (dosage varies per person), taking this is going after REM and Deep sleep stages (@ body healing), and other things. 
Reishi extract- 2X per day (anti-androgen) follow manufacturers dosing guidelines though, the higher the polysaccharides the stronger anti-androgen. Like this one below, it's organic and 35% polysaccharides. 
Green Tea Extract - 2x per day @ 45% to 90% EGCG 100mg to 200mg capsules each taken 2x per day, ideally taken with Reishi. I prefer decaffeinated GTE (I drink coffee so I don't need the extra caffeine). I attached a picture as an example, though this product is expensive. I look for minimal additives when sourcing suppliments, like no silica, silicone dioxide (which basically is the same as silica) maltodrexin, which stimulates insulin.

Technically, MSM stimulates the stat5 pathway which facilitates phosphorylation and the nuclear translocation and DNA binding...in other words it helps with breast growth. MSM also stimulates prolactin and enhances GH (growth hormone)lol. 

Additionally, there's no reason to take a break (e.g. 5/2 or 6/1) because DHT doesn't take a day off. Nor is there ANY reason to follow the cis-female menstrual cycle because cis-males don't have ovaries. Following the menstrual cycle is essentially running something like PM or estradiol for the 14 days followed by running PC (progesterone cream) for the remaining cycle stopping PC before the females next period (menstruation), it's pointless and not in the best interest of growing breasts on this forum. I used to promote doing the 5/2 cycle years ago to give receptors a chance to reset, I no longer support that theory. 

I'll be adding my topical program and other supplements asap. 

Many, many thanks to you Lotus for all the work and inspiration you provide.  It is truly appreciated.

I burned an hour searching, so will ask about recommendations for sourcing the MSM. Above, you mentioned  ( MSM 1-3g per day)  and I am wondering if you recommend the pill form or the powder?  Regardless, any recommendations on brand?  I know that your research is top notch and know that the stuff you source will be as well.

Thanks for all you do and your vast knowledge on the topics you post. 

Cheers,

Tiffany

[CM213]

I had used the same brand as the red reshi in the above post for msm. I did not notice anything negative or positive about it. Honestly didn't know if it was really working or not or what was working or not. It's just one of those things that supports the nbe and you hope it is doing what it is supposed to do, and you hope you're giving your body enough of a supply of it for it to be effective. 

Like bodybuilding taking bcaa's and glutamine, protein and creatine. Some things are a bit more obvious as to them working like protein or creatine (which I would.compare to pm or hrt) will the supporting supplements like branch chain amino acids, and glutamine and fish oils etc you (which would be like red reshi and MSM and green tea extract and all the other supporting supplements of nbe) you really kind of hope you're giving you body enough of a continued supply for the desired outcome

[SweetO]

Wow, thank you L for giving us such good information. It is like solving a puzzle, step by step 

So vit D is key too! I've got a question. Do you think its best to take it daily than every 15 days? I am thinking in changing my prescription. Right now I am taking every two weeks a dose. Apparently it is a high dose but I read somewhere your body cannot take it all of it .... and I do take magnesium to help with absorption, but anyway  My outcome is steady. I am in the optimal range currently but I know when you stop taking it sooner or later the body will deplete vit D again. That's my main concern. 

Oh about the DHT part. The more I get to know this damn hormone the more I hate him


Hugs y'all and good night from Barcelona!

[wee2er]

@ SweetO - You can overdose on Vit D especially if you are taking a high dose, and that comes with it's own dangers!
I decided to add Vit D 10,000/day, then after my quarterly blood checks (I have bloods checked for an existing medical condition) my blood docs hit the roof with me and gave me a right bollocking LOL
Needless to say I stopped it and now take 10,000 twice a week which seems to keep my Vit D levels up and seems to be the right amount for me.

[SweetO]

@ SweetO - You can overdose on Vit D especially if you are taking a high dose, and that comes with it's own dangers!
I decided to add Vit D 10,000/day, then after my quarterly blood checks (I have bloods checked for an existing medical condition) my blood docs hit the roof with me and gave me a right bollocking LOL
Needless to say I stopped it and now take 10,000 twice a week which seems to keep my Vit D levels up and seems to be the right amount for me.

Wow! So there's a possibility/risk to overdose it. Thank you I didn't know it!

[SweetO]

L! I had some notes from 2015 you posted about in Breastnexus and I just want to make sure if my notes (copy pasted to my NBE notes  back then) if you resonate with this? ...

"PC applied directly to the breasts (thinly applied) 1/4 teaspoon is about 20m to 25mg. I would advise to use PC at bedtime. I think this will help two fold, PC is also an anti androgen. That's 1 (number 2) is helping with growth hormone released in the first two hours of sleep, PC helps with sleep.

If you have an estrogenic cream use it when applying PC. Make sure it's less then amount of PC you use. PC combined with E2 stimulates more tissue growth than if used separately (paper posted in Hrt pharmacokinetics thread). It takes about 15 minutes for PC to dry. Don't put PC on the areolas, it will produce brown spots (freckles)"


I was looking for transdermal tips and I came across with this statement you made to a forum member called LanaG. 

 It makes sense to use both at a time but makes me wonder: when? right after ovulation? and how many days? 


PS: got DHEA finally. I'll start using 15mg for two months and see how it goes. I've read the libido thing is real