[Grayson123]

A tablespoon of fenugreek seeds is nowhere near the amount used in a typical Indian dish. The seed is one of many components of spice powders and there’s one teaspoon max of the entire spice mix used in a typical serving of a curry or stir fry. 

Fenugreek leaves are used as a vegetable sometimes but they have much, much lower concentrations of phytoestrogens than the seeds.

[surferjoe2007]

Saponins” is kind of like “essential oils” in that I hope you mean fenugreek or shatavari or else it could be something else entirely.  1200 mg is a safe low amount of either with 50% saponins.  You can go up to 2400 mg if there aren’t any side effects.  Maybe a little further such as 3,000-3,600 mg again if there aren’t side effects.  Though it might not do much more.  If you do good side effects then a few months on the foods may help before increasing again.  Same for other herbs.  If you have hypoglycemia then don’t use any amount of fenugreek or shatavari

Sorry, this advice is reckless. Fenugreek lowers insulin...fast. Suggesting such amounts to women can bottom out a female's blood sugar level in no time flat. You've suggested this course before and a good friend of mine followed your advice and passed out and wound up in the hospital requiring stitches...good thing she wasn't driving, do you remember this joe? And as I cautioned back then about going over the recommended amounts you're still suggesting these crazy amounts.

"A cautionary tale for sure, herbs do carry risks. As with anything, always check with your primary care physician. And a general rule: do not exceed the recommended dosage. The higher (or more) the better theory for supplements is completely false."
https://www.breastnexus.com/showthread.php?tid=23119
 (you're response is on page 2, joe) 

Fenugreek increases estradiol
https://www.breastnexus.com/showthread.php?tid=26172

Per the study:

The investigational product contained 300 mg of libifem, a standardized extract of T.foenum-graecum (fenugreek) seed extract [dry concentrate 33:1] equivalent to 9.9 g dry herb, standardized to a minimum 50% saponin glycosides.

foenum-graecum seed extract was also associated with a significant increase in E2 levels.(Simon, 2011) 

Study participants underwent follicular blood tests on day 7-9, (though not all did).....thus the data on increased estradiol. It makes sense (to me) taking FG in follicular.....vitex in luteal would work too. And in my opinion Vitex is a generic version of Prozac.....which will increase PRL (and it does).  

Fenugreek lowers progesterone and raises estradiol followed by prolactin.

Hey Lotus
I thought since FG raises estradiol, wouldn't that be taken when E rises? But you're also saying it raises P-- so I am a bit confused lol (sorry) this whole time I thought FG worked on E and should be taken during follicular?

Do you think FG extract should be cycled the same way because it would have the same effect? I have been considering Fenu extract, flaxseed and hops oils (all topical)

Hey there missB,

The science from the study indicates estradiol (in the second month) was raised by 50%(my calculations) @ 600 mg a day for two menstrual cycles. Btw, FG needs to be at least 50% steroidal saponins. (NOTE-that's not a misprint, only 600 mg was used).

 steroidal saponins reported to exhibit estrogenic effects including binding to E2 receptors and inducing the expression of E2 responsive genes (Sreejaet al., 2010). 

It raises prolactin yes, though not as significant as estradiol. From the study, FG lowers cholesterol, SHBG, progesterone and FSH (follicle stimulating hormone). It also raises LH (luteinizing hormone @ 41%)......thus the need for additional 5 AR inhibitors.

To me, FG needs to be in the first half and Vitex in the second half. I'll have to adjust the supplement info about FG lowering progesterone. Alternatively, I'd take FG with a conversion supplement (pro-aromatase) considering what it does to FSH, which synthesizes aromatase. I'm excited about a new aromatase approach using EPO and peanut oil, though I'm looking for an alternative for those with peanut allergies. What the 2 combination does is its binding ability in EGF (epidermal growth factor). I'll post more info on the X thread. 

Topical FG is OK (though much DHT is in the skin). Use a good skin penetrator that inhibits 5 Alpha Reductase (inhibits DHT) too.....EPO (evening primrose oil) could work. The study size was 80 premenopausal women.  

Palmdef, more than likely your issue is hidden in DHEA (though not listed, I'm confident having read/analyzed many lab results to know (or recognize) the pattern based on what youve already shared. Your results are similar to women with pcos or hirsute woman…not identical, but similar. Low Estradiol, higher androgens, chin hair etc, though much is driven by your weights lifting, so your body is sensing the increase in T most likely driven by an increase in IGF-1. Inhibiting DHEA, lowering SHBG and raising estradiol is your main goal. Fenugreek helps lower SHBG and raises Estradiol, per the study only 600 mg fenugreek was used. In addition you can also add a pro-aromatase supplement to help synthesize fenugreek during follicular phase, e.g. forskolin or ginseng. For luteal I'd recommend still using 600mg of fenugreek alongside micronized progesterone cream. 

If you require even stronger anti-androgens I'll be sharing new information in my thread later today. Apologies for the intrusion in your thread, I think you deserve the correct information. I'm adding this study because you'll see DHEA-S and DHEA are the major androgens in females followed by androstenedione (A), testosterone (T), and dihydrotestosterone (DHT) in descending order of serum concentration.

Androgen production in women 
Henry G Burger. Fertil Steril. 2002 Apr. 
Abstract 

Objective: To describe the sources, production rates, circulating concentrations, and regulatory mechanisms of the major androgen precursors and androgens in women. 

Design: Review of the major published literature. 

Result(s): Quantitatively, women secrete greater amounts of androgen than of estrogen. The major circulating steroids generally classified as androgens include dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione (A), testosterone (T), and dihydrotestosterone in descending order of serum concentration, though only the latter two bind the androgen receptor. The other three steroids are better considered as pro-androgens. Dehydroepiandrosterone is primarily an adrenal product, regulated by adrenocorticotropic hormone (ACTH) and acting as a precursor for the peripheral synthesis of more potent androgens. Dehydroepiandrosterone is produced by both the ovary and adrenal, as well as being derived from circulating DHEAS. Androstenedione and testosterone are products of the ovary and the adrenal. Testosterone circulates both in its free form, and bound to protein including albumin and sex steroid hormone-binding globulin (SHBG), the levels of which are an important determinant of free testosterone concentration. 

Conclusion(s): The postmenopausal ovary is an androgen-secreting organ and the levels of testosterone are not directly influenced by the menopausal transition or the occurrence of menopause. Dihydrotestosterone (DHT) is primarily a peripheral product of testosterone metabolism. Severe androgen deficiency occurs in hypopituitarism, but other causes may lead to androgen deficiency, including Addison's disease, corticosteroid therapy, chronic illness, estrogen replacement (leads to elevated SHBG and, therefore, low free testosterone), premenopausal ovarian failure, or oophorectomy.

I’ve been using a little more and I’m a small person.

Here’s a rat study with the 77.5 kg human (average woman) equivalent of 3,230 mg saponins (6,460 mg 50% saponin) with various benefits:
https://pubmed.ncbi.nlm.nih.gov/8539775/

https://pubmed.ncbi.nlm.nih.gov/?term=fenugreek has 1,634 fenugreek studies.  I’ve never found harm at any amount but you’re free to browse through them.  The closest thing to harm I can remember is rabbits eating a diet of 100% fenugreek went infertile, I’m guessing from the high hormones, similar to birth control.  Many of the linked studies have amounts.

She asked what the max is, so I said 2,400 mg 50% saponin, maybe 3,000-3,600 mg.  After trying less first and confirming no negative effects.  I bring up 3,000-3,600 mg because it’s unlikely to hurt at all, unlike even 1 capsule of PM which has caused trouble in programs much more often.  Especially if not balanced with progesterone or to balance out an existing high progesterone / low estrogen imbalance.  The main downside to 3,000-3,600 mg is that it might not help much more.  It’s a safer bet than diving into the more problematic PM.  Many forum programs have used 2,400 mg.  Many have also used 1-3 tbsp. of the whole seed.  The forum search tool should pick up those.  I’ve also talked directly to several doing the same. Fenugreek has multiple health benefits including balancing hormones, preventing cancer and improving mood.  For most people besides hypoglycemics reducing blood sugar is also a health benefit and it does not do so excessively.  Most women using it feel better and have better health rather than getting hormonal problems as with other nbe ways.

[surferjoe2007]

A tablespoon of fenugreek seeds is nowhere near the amount used in a typical Indian dish. The seed is one of many components of spice powders and there’s one teaspoon max of the entire spice mix used in a typical serving of a curry or stir fry. 

Fenugreek leaves are used as a vegetable sometimes but they have much, much lower concentrations of phytoestrogens than the seeds.

Fenugreek can be both a spice and the dish which is seasoned with other spices.  Here is one:
https://www.archanaskitchen.com/methi-da...s-stir-fry

When I Googled it I found more recipes than I could count with fenugreek seeds as the main part.  The above link has 5,740 ratings.  I’m not sure if I’ve ever seen such a popular recipe.  Average is 5 stars.  It has 1 tbsp. fenugreek seeds per serving.  The lunch they suggest has 4 dishes including this one for around 10,000 mg fenugreek (whole seed not extract), 9,000 mg dry spices and a very large amount of fresh herbs.  In India this is just called food.

[Palmdef]

 I have just recently started lifting again and cleaning up my diet, which I’m aiming for high protein and low carb (working on growing the butt again too). I’m a pretty lacking 32B, 26f and looking to go as big as I can really. 
Really inspired and excited by all the journeys shared here, any help is appreciated x

Palmdef, I think you'll be okay with adding more protein, from the science I've seen on protein synthesis and its pathway can help with breast growth. But you'll need to add MSM and vitamin D3 to make this combination work more efficiently. Those two together have a synergistic combination in breast growth with attached science. I would also recommend with the added protein you'd consider using an anti-androgen. 

Gender differences in metabolism; nutrition and supplements
M A Tarnopolsky. J Sci Med Sport. 2000 Sep.
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Abstract
For many decades researchers did not consider that there were any differences between the genders in the metabolic response to exercise. As a result, nutritional recommendations and exercise training prescriptions have not considered the potential for gender specific responses. More recently, we and others have demonstrated that females oxidize proportionately more lipid and less carbohydrate during endurance exercise as compared to males. The oxidation of amino acids is similarly lower in females as compared to males during exercise. These gender differences are partially mediated by a higher estrogen concentration in females. Specific areas where there are gender differences in nutritional/supplement recommendations include carbohydrate (CHO) nutrition, protein requirements and creatine (CRM) supplementation. We have shown that females do not carbohydrate load in response to an increase in dietary carbohydrate when expressed as a percentage of total energy intake (i.e., 55-75%), however if they consume >8 g CHOxkg(-1)xd(-1), they show similar increases as compared to males. Top sport male and female athletes require somewhat more dietary protein as compared to sedentary persons. The maximal increase is approximately 100% for elite male athletes and approximately 50-60% for elite female athletes. Fortunately, most athletes habitually consume this level of protein intake. We have recently demonstrated that females show a lesser increase in lean body mass following acute CRM loading as compared to males. Females also did not show reductions in protein breakdown in response to CRM loading, whereas males did. In the future I expect that there will be further research from which gender specific nutritional/supplement recommendations

Thank you so much for the comprehensive information, lotus! Seriously appreciated, I have always speculated that I have too much androgen, and as of late with the increased chin hairs and potential hair thinning at my crown I’m going to go with that route until I can see my doctor for a test again. I’m currently taking 1200 50% saponins of shatavari, around 800mg of raw maca (both once a day), and will take 600 mg of fenugreek- would you recommend fenugreek over saw palmetto? I bought both but have used neither. I do currently take MSM and vitaminD3, but the max I’m able of MSM is 1000mg or I get a terrible headache that nothing can help with.

[Lotus]

Thank you so much for the comprehensive information, lotus! Seriously appreciated,

You're quite welcome 

 I have always speculated that I have too much androgen, and as of late with the increased chin hairs and potential hair thinning at my crown I’m going to go with that route until I can see my doctor for a test again. I’m currently taking 1200 50% saponins of shatavari, around 800mg of raw maca (both once a day), and will take 600 mg of fenugreek- would you recommend fenugreek over saw palmetto? 

Saw Palmetto will help inhibit DHT, in comparison to other stronger anti-androgen SP inhibits DHT at 32% in male prostate glands. No, you'll need something much much stronger, that'll even improve acne, improve estrogen metabolism and inhibit DHT like in pharma class…I can recommend one after uncovering recent research and its been flying under the radar so to speak….it's called DIM. I'll be attaching the research here shortly. 

I bought both but have used neither. I do currently take MSM and vitaminD3, but the max I’m able of MSM is 1000 mg or I get a terrible headache that nothing can help with.

I believe the problem is the SP, more directly the beta-sisterol in saw palmetto, i had similar issues with headaches and stomach cramps, try dropping the SP and see if that helps. Have you seen my posts on MSM and HIIT?, let me know and I'll link them for you, it's a perfect fit for you and your weight lifting. 

The fenugreek study I posted used only 600mg to increase estradiol, I don't know why that amount is hard for some people to come to grips with, and the fact it's a human study (not a rat study). 

And of course if you can't use DIM certainly try green tea extract w/ EGCG (sourcing the highest percentage possible) 

Or reishi mushrooms 

Both inhibit DHEA/DHT in the 80-90% range

[Palmdef]

No, you'll need something much much stronger, that'll even improve acne, improve estrogen metabolism and inhibit DHT like in pharma class…I can recommend one after uncovering recent research and its been flying under the radar so to speak….it's called DIM. 

I would love to be linked to your thread on MSM and HIIT! I’m still struggling to navigate this site in my mobile browser  should I be cycling the DIM?

 i acquired some DIM supplements and have been taking 100mg a day for the past week and a half- my period has just started, and there were significantly less severe and fewer cramps which I am excited about! Breasts feel very full and sore for longer than I’m used to for PMS, normally it’s 5 days but I think I’m on day 10, even the boyfriend has commented on how good my breasts look. The downside is my skin has broken out pretty severely when acne is normally not an issue for me minus a minimal hormonal breakout, but I have done some reading on DIM detox and am hopeful sticking it out will clear my skin back up. Holiday sweets haven’t been helpful I’m sure.

[Lotus]

I would love to be linked to your thread on MSM and HIIT! I’m still struggling to navigate this site in my mobile browser  should I be cycling the DIM?

Sure, I'm posting here ro make it easier for you.

Hi Ladies, I shared the DIM information the other day in my program thread @ Project X, I'm attaching the information here for reference too. I'm also attaching DIM research for PCOS. DlM improves estrogen metabolism, DIM shifts production of the dangerous estrogen metabolite 16a-hydroxy in favor of the beneficial (or healthier) 2-hydroxy 2-OH metabolite. So it's hypothesized that the 2 OH pathway over 16α-OH pathway (which is inversely associated with breast cancer risk) is a safer option.


The promising effect of linagliptin and/or indole-3-carbinol on experimentally-induced polycystic ovarian syndrome
Ahmed M Kabel et al. Chem Biol Interact. 2017.
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Abstract
Polycystic ovarian syndrome (PCOS) is one of the most common medical conditions that lead to female infertility worldwide. The aim of this study was to assess the effect of linagliptin and/or indole-3-carbinol (I3C) on PCOS in female rats. Fifty female Wistar rats were randomly allocated into five equal groups: Control group; Letrozole-induced PCOS group; Letrozole + Linagliptin group; Letrozole + I3C group and Letrozole + Linagliptin + I3C group. Body weight, body mass index, Lee index and ovarian indices were determined. Plasma levels of luteinizing hormone (LH), free testosterone, estradiol, progesterone, prolactin, fasting blood glucose (FBG) and fasting plasma insulin were measured. Quantitative Insulin Sensitivity Check Index (QUICKI) was calculated. Tissue antioxidant status, transforming growth factor beta 1 (TGF-β1), tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10) and Nrf2/HO-1 content were assessed. Histopathological and immunohistochemical examination of the ovaries were done. Linagliptin and/or I3C induced significant decrease in tissue TGF-β1, TNF-α, IL-10, plasma free testosterone, luteinizing hormone, progesterone, estradiol, FBG and insulin levels associated with significant improvement of insulin resistance whereas tissue Nrf2/HO-1 content and antioxidant enzymes were significantly increased compared to PCOS group. In addition, final body weight, final body mass and Lee indices were significantly decreased compared to PCOS group. Also, there was significant improvement of the ovarian morphology compared to PCOS group. This improvement was significant with linagliptin/I3C combination compared to the use of each of these drugs alone. In conclusion, linagliptin/I3C combination might represent a beneficial therapeutic modality for amelioration of PCOS.

DIM is Diindolylmethane. It is an anticarcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, although the atomic compositions of the two substances are quite different. Taken together with our published reports of the estrogen agonist activities of DIM, the present results establish DIM as a unique bifunctional hormone disruptor. To our knowledge, DIM is the first example of a pure androgen receptor antagonist from plants.

http://www.jbc.org/content/278/23/21136.full

From the study above on DIM I pulled certain paragraphs of information to highlight. Two main points: DIM inhibits DHT, and DIM is similar to Casodex, which is similar to ??? drum roll please: the prescription anti-androgen Bicalutamide. 

The effects of DIM on human prostate cancer cell growth were examined using LNCaP and PC-3 cells. After a 96-h treatment, DIM produced a concentration-dependent inhibition of LNCaP cell proliferation with maximal inhibition of 70% at 50 μm.

DIM strongly inhibited DHT induction of androgen-responsive genes by more than 50% at 1 μm and more than 90% at 10 μm in both promoter constructs 

Cyproterone acetate and Casodex, two well known antiandrogens, were used as positive controls. DIM and Casodex exhibited similar binding affinity for the AR.

Because both DIM and Casodex act as pure antiandrogens, we compared the structures of these ligands more closely.
the two ligands are remarkably similar in conformation despite their considerable difference in atomic compositions

DIM is remarkably similar in molecular geometry and surface charge distribution to the well established synthetic antiandrogen, Casodex. Our investigation, leads to the conclusion that DIM is a strong, pure androgen antagonist.

______________________________

The following is my analysis, or model of how DIM being a pro-aromatase, and it works following the CREB-binding protein

"Cyclic AMP response element binding protein (CREB) activates transcription of cAMP response element (CRE)-containing promoters following an elevation of intracellular cAMP"...which is basically a second messenger and if you've read this thread no doubt you've seen it posted many times lol, it's a pro-breast pathway once inside the cytoplasm. 

How it relates to DIM is the hormone receptors are transferred to common compartments located in the euchromatin region and form a complex with co-activators…I see a window, or an opening. And judging how the rat study below shows how the CYP1B1 cytochrome opens the door for enhanced E2 production I'm feeling more confident the window opening got a little bigger. 

The formation of these nuclear foci is thought to provide platforms for the interaction of nuclear receptor and co-activators (38). Liganded steroid hormone receptors are transferred to common compartments located in the euchromatin region and form a complex with co-activators, such as steroid receptor coactivator 1, transcriptional intermediary factor 2, and CREB-binding protein, which are also accumulated in the same subnuclear compartments. For the AR, CREB-binding protein was found to be essential for foci formation, and the process of compartmentalization is essential for full transactivation 
https://www.jbc.org/article/S0021-9258(20)73423-X/fulltext

Dietary indole-3-carbinol promotes endometrial adenocarcinoma development in rats initiated with N -ethyl- N ′-nitro- N -nitrosoguanidine, with induction of cytochrome P450s in the liver and consequent modulation of estrogen metabolism 
https://academic.oup.com/carcin/article/...ogin=false

In the assays of estradiol hydroxylase activities in the liver, dietary I3C increased both 2- and 4-hydroxylase activities, in particular the latter. These results strongly suggest that the induction of the CYP 1 family by I3C is linked to modulation of E2 metabolism. 

Meaning DIM can enhance E2 production 

I have more information on HIIT/MSN, but this is a good place to start. 

Good conversation going here, (nice link Ella). 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
http://www.ncbi.nlm.nih.gov/pubmed/11086655