Breast Growth For Genetic Males

Quote:A primary feature of the androgen backdoor pathway is that 17α-hydroxyprogesterone (17-OHP) can be 5α-reduced and finally converted to 5α-dihydrotestosterone (DHT) via an alternative route that bypasses the conventional[3] intermediates androstenedione and testosterone.[1][6]

(07-08-2020, 08:39 AM)Nefertity Wrote: [ -> ]

(07-08-2020, 05:58 AM)Lotus Wrote: [ -> ]Hi Nefertiddy, 

I'm not a fan of BO (i had horrible side effects). Here's one of many issues I have with BO, (and I posted on this 5-6 years ago) we don't know when cattle are harvested. Meaning cows (heifers) have (roughly) a 21 day estrous cycle. 


Each cycle consists of a long luteal phase (days 1-17) where the cycle is under the influence of progesterone and a shorter follicular phase (days 18-21) where the cycle is under the influence of estrogen. The cycle begins with standing heat, or estrus. This time of peak estrogen secretion can last from 6 to 24 hours, with ovulation occurring 24 to 32 hours after the beginning of estrus.
https://beef.unl.edu/learning/estrous.shtml

Here's questions we should ask:

1)Is the BO from 100% grass fed/grass finished, free of antibiotics, pesticides, hormones, and GMO. 2) When was livestock harvested?, meaning when in an estrous cycle (this is most likely unobtainable). 
3) How long did the BO sit around before being frozen and dissected. 
4) Is the livestock subjected to synchronization?. This process shortens the breeding period to less than 5 days, instead of females being bred over a 21-day period, depending on the treatment regimen.

Ovaries from non-pregnant cows and heifers, obtained shortly after slaughter, were extracted with ethyl acetate and then defatted in cold 70% methanol.

4.33 μg. of progesterone  
0.79 μg- of Δ4-pregnene-20β-ol-3-one per gram of ovarian tissue. 
A trace of Δ4-androstene-3,17-dione or Δ4-pregnene-20α-ol-3-one and a very polar material were also detected.

I know BO has 17 β-estradiol (E2), it's difficult to quantify how much based on cell cultures though. Rather, we can say Testosterone is being synthesized (converted) to Estrogen by way of aromatase, which raises estrogen. 

But...seeing how short of time estrogen is stimulated in BO it's safe to say BO consists of more progesterone than estrogen. 

But when to supplement w/BO?. I'm gonna say in Luteal. 

The decision is up to you to Nefertiddy, try and see how it works. Though don't follow the old tired mantra of taking massive amounts. 2 per day to start works ok. 

wow...

The timing of slaughter is a very good point, I highly doubt that there is any consideration taken to the cycle of the cows... I can imagine that would complicate production and if they did the big brands would definitely advertise it. Maybe this could explain why some end up with androgenic effects (acne seems to be common) while others are greatly successful with it.

It seems to be sold out everywhere so I have some time to consider it. This was great insight, thank you so much!

(07-07-2016, 10:26 PM)Lotus Wrote: [ -> ]Information worth repeating,


Growth Hormones creates new receptors, lactate triggers HGH. HIIT also triggers repair peptides, which helps fight the free radicals, in other words tissue repair. You could supplement pre or post workout, imo supplementing pre-workout would synergistically work with HGH. Make sleeping part of the fasting process, create your own schedule to manage time limits.

Mechanism of Action: Hormones with Cell Surface Receptors
http://www.vivo.colostate.edu/hbooks/pat...rface.html

(05-06-2015, 08:19 PM)Lotus Wrote: [ -> ]

(03-06-2015, 04:42 AM)Lotus Wrote: [ -> ]MSM does many things, top of the list is breast cancer protection. Indirectly to NBE, MSM upregulates growth hormone, which is essential for breast growth as we know. If we take a lead from this first study we see possible link towards NBE, but, it leans towards favoring males in the liver. I'll look further though.

MSM enhances GH signaling via the Jak2/STAT5b pathway in osteoblast-like cells and osteoblast differentiation through the activation of STAT5b in MSCs.
Joung YH1, Lim EJ, Darvin P, Chung SC, Jang JW, Do Park K, Lee HK, Kim HS, Park T, Yang YM.
Author information
Abstract
Methylsulfonylmethane (MSM) is a naturally occurring sulfur compound with well-known anti-oxidant properties and anti-inflammatory activities. But, its effects on bone are unknown. Growth hormone (GH) is regulator of bone growth and bone metabolism. GH activates several signaling pathways such as the Janus kinase (Jak)/signal transducers and activators of transcription (STAT) pathway, thereby regulating expression of genes including insulin-like growth factor (IGF)-1. GH exerts effects both directly and via IGF-1, which signals by activating the IGF-1 receptor (IGF-1R). In this study, we investigated the effects of MSM on the GH signaling via the Jak/STAT pathway in osteoblasts and the differentiation of primary bone marrow mesenchymal stem cells (MSCs). MSM was not toxic to osteoblastic cells and MSCs. MSM increased the expression of GH-related proteins including IGF-1R, p-IGF-1R, STAT5b, p-STAT5b, and Jak2 in osteoblastic cells and MSCs. MSM increased IGF-1R and GHR mRNA expression in osteoblastic cells. The expression of MSM-induced IGF-1R and GHR was inhibited by AG490, a Jak2 kinase inhibitor. MSM induced binding of STAT5 to the IGF-1R and increased IGF-1 and IGF-1R promoter activities. Analysis of cell extracts by immunoprecipitation and Western blot showed that MSM enhanced GH-induced activation of Jak2/STAT5b. We found that MSM and GH, separately or in combination, activated GH signaling via the Jak2/STAT5b pathway in UMR-106 cells. Using siRNA analysis, we found that STAT5b plays an essential role in GH signaling activation in C3H10T1/2 cells. Osteogenic marker genes (ALP, ON, OCN, BSP, OSX, and Runx2) were activated by MSM, and siRNA-mediated STAT5b knockdown inhibited MSM-induced expression of osteogenic markers. Furthermore, MSM increased ALP activity and the mineralization of MSCs. Taken together, these results indicated that MSM can promote osteogenic differentiation of MSCs through activation of STAT5b.



Growth hormone pulse-activated STAT5 signalling: a unique regulatory mechanism governing sexual dimorphism of liver gene expression.
Waxman DJ1.
Author information
Abstract
Growth hormone (GH) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release; this release is intermittent in male rats and nearly continuous in females. Comparisons of liver nuclear protein tyrosine phosphorylation in male and female rats have led to the discovery that the liver transcription factor STAT5b is tyrosine phosphorylated in male but not female rats in response to GH pulses. Intermittent plasma GH pulses trigger a rapid and repeated tyrosine phosphorylation and nuclear translocation of liver STAT5b in intact male rats, while the more continuous pattern of GH exposure down-regulates the STAT5b signalling pathway in female rat liver. The central importance of STAT5b for the physiological effects of GH pulses has been verified using a mouse gene knockout model. STAT5b gene disruption leads to a major loss of multiple sexually differentiated responses associated with the sexually dimorphic pattern of pituitary GH secretion. Male-characteristic body growth rates and male-specific liver gene expression are decreased to wild-type female levels in STAT5b-/- males, while female-predominant liver gene products are increased in males to near female levels. STAT5b is thus a liver-expressed, latent cytoplasmic transcription factor that undergoes repeated tyrosine phosphorylation and nuclear translocation in response to intermittent plasma GH stimulation, and is a key intracellular mediator of the stimulatory effects of GH pulses on male-specific liver gene transcription. Other studies indicate, however, that STAT5a and STAT5b are both required for constitutive expression in female, but not male liver, of certain GH-regulated CYP enzymes. GH activation of both STAT5 proteins, which in turn form distinct homodimeric and heterodimeric DNA-binding complexes, is thus an important determinant of the sex-dependent and gene-specific effects that GH has on the liver.

I think it makes sense to take MSM after a high intensity workout, (biotin too, for its abilty to break down carbs). But because MSM induces binding of STAT5 to the IGF-1R and increases IGF-1 and IGF-1R promotes these activities you'd have to give MSM considerable attention for after workout repair. I like the 12-14 hour intermittent fast, followed by High-intensity Interval Training (HIIT) , that's short bursts of intense work followed by less intense activity or rest.


Growth hormone signaling in human adipose and muscle tissue during "feast and famine"; Amplification of exercise stimulation following fasting compared to glucose administration.

Conclusions: This study demonstrates that fasting and exercise act in tandem to amplify STAT-5b target gene expression (SOCS and CISH) in adipose and muscle tissue in accordance with the "feast and famine hypothesis"; the adipose tissue signaling responses which hitherto have not been scrutinized may play a particular role in promoting FFA mobilization.

http://www.eje-online.org/content/early/...1157.short


Fasting and fitness boost human growth hormone

Intermittent fasting for periods ranging from 12-24 hours along with high intensity exercise has a positive effect on boosting human growth hormone (HGH). HGH is a very important protein-based hormone that is produced by the pituitary gland. HGH enhances the cellular repair processes that allow us to age with grace. HGH regulates metabolism to burn fat, build muscle, and slow down the negative effects of stress.

Researchers at the Intermountain Medical Center Heart Institute found that men who had fasted for 24 hours had a 2000% increase in circulating HGH. Women who were tested had a 1300% increase in HGH.

A 2009 study in the British Journal of Sports Medicine showed that lactic acid accumulation helps to trigger HGH. Lactic acid is only produced in response to intense anaerobic training. Aerobic training is not intense enough to produce the kind of lactate triggering of HGH.

Low-intensity, long duration aerobic training is catabolic in nature. This means that it produces lots of free radicals without promoting significant amounts of repair peptides, enzymes and hormones. The net effect is a wearing down of bodily resources.

High-intensity training also produces free radicals but it triggers an abundance of repair peptides, enzymes and hormones to be released. The net effect of this is healthy tissue repair and favorable effects on body composition and anti-aging qualities.

Learn more:  http://www.naturalnews.com/034704_interm...z3cAB6XEkK

Effects of growth hormone on adipose tissue

growth hormone on adipose tissue.
Carrel AL1, Allen DB.
Author information
Abstract
Physiological effects of growth hormone (GH) extend beyond the stimulation of linear growth. These include important metabolic effects upon adipose tissue. GH affects both proliferation and differentiation of preadipocytes, although this varies between clonal cell lines and preadipocyte cultures. Both preadipocytes and mature adipocytes possess specific GH receptors. GH may mediate its actions via these receptors, but some effects are indirectly mediated through the GH-mediated secretion of insulin-like growth factor-I (IGF-I) within adipose tissue. GH promotes lipolysis via inhibition of lipoprotein lipase, which hydrolyzes triglycerides in the circulation to make them available for triglyceride accumulation in adipose tissue. GH also stimulates hormone sensitive lipase (HSL), the rate-limiting step for release of stored triglyceride in adipocytes (lipolysis). As GH becomes utilized for various "non-growth" concerns (see Figure 1), awareness of the metabolic effects on adipocytes is important to understand the clinical effects seen with GH therapy.
http://www.ncbi.nlm.nih.gov/pubmed/11086655

lactate is a product of aerobic glycolysis that can be used by neurons as an energy substrate. Here we report that in neurons L-lactate stimulates the expression of synaptic plasticity-related genes such as Arc, c-Fos, and Zif268 through a mechanism involving NMDA receptor activity and its downstream signaling cascade Erk1/2. L-lactate potentiates NMDA receptor-mediated currents and the ensuing increase in intracellular calcium. In parallel to this, L-lactate increases intracellular levels of NADH, thereby modulating the redox state of neurons. NADH mimics all of the effects of L-lactate on NMDA signaling, pointing to NADH increase as a primary mediator of L-lactate effects. The induction of plasticity genes is observed both in mouse primary neurons in culture and in vivo in the mouse sensory-motor cortex. These results provide insights for the understanding of the molecular mechanisms underlying the critical role of astrocyte-derived L-lactate in long-term memory and long-term potentiation in vivo. This set of data reveals a previously unidentified action of L-lactate as a signaling molecule for neuronal plasticity.

(03-09-2022, 09:24 AM)Lotus Wrote: [ -> ]Other pics-the bare boob was a post pumping pic, something Lara might appreciate from back in the day, I don't pump anymore though.

(03-09-2022, 09:57 AM)HelloDiDi Wrote: [ -> ]

(03-09-2022, 09:24 AM)Lotus Wrote: [ -> ]Other pics-the bare boob was a post pumping pic, something Lara might appreciate from back in the day, I don't pump anymore though.

Very nice pics again. Is that a waist trainer/corset you're wearing btw? You said your band has gone down to 36, due to weight loss? I've lost some too and I think very soon nearly all 38's might fit the best. My currently best fitting bra I keep on tightest setting as it gives such nice lift and its kinda stretchy material. Non stretching stuff, I'm not sure as some manufacturers just do their own thing.

Its interesting how I seem to have almost opposite shape than you btw, I mean root width + height. I envy that projection.