Thanks so much Lotus for your new posts today. POM

thanks Pom, I appreciate that, have a good night.

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/2015/06/01/EJE-14-1157.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_intermittent_fasting_fitness_HGH.html#ixzz3cAB6XEkK

Effects of growth hormone on adipose tissue
http://www.ncbi.nlm.nih.gov/pubmed/11086655

This is VERY well written. I've never come across these concepts summarized as well as they are in this article. Thanks for all of your research. It's invaluable... and gives me something to do when the dog wakes me up in the middle of the night!

This is VERY well written. I've never come across these concepts summarized as well as they are in this article. Thanks for all of your research. It's invaluable... and gives me something to do when the dog wakes me up in the middle of the night!

Lol @ the pooch, I'm glad you found it helpful.

Speculating on how the brain/liver CYP enzyme connection to feminization is a ways off I believe, it looks good in a lab at this point using CYP2B9. Although human CYP2C9 looks promising.

So, at this point this theory is like saying how nicotine acts like GHB (mda) in the brain, although that statement could be true too, two different enzymes though.

I'm not throwing in the towel just yet, STAT5 protein is even metabolized with prolactin, so MSM is still a viable option for the growth hormone link to the hypothalamus connection......and feminizing......aka (ER-alpha).....just have to find the right access (CYP enzyme).

What's interesting about inhibiting CYP ligands are the fact (or, in fact lol) they increase drug metabolism (actually, the decrease clearance). But, for our purpose of discussion, the action is quite literally seen as an upregulation. And a strong inhibition of CYP's can be over 80%, (or, over a 5 fold increase).

Greetings loved ones,


In this small study, 12 women with high progesterone levels exhibited higher breast tissue levels of estradiol compared with fat tissue in luteal phase, another 12 women with low levels of progesterone had low breast tissue estradiol too. It reinforces that progesterone has a big impact on breast tissue, especially in the luteal phase.

This also backs up that taking PM all cycle is a mistake.........my opinion, FWIW. And a corresponding increase in what we know as swelling, again.....imo.


Increased extracellular local levels of estradiol in normal breast in vivo during the luteal phase of the menstrual cycle
http://joe.endocrinology-journals.org/co...3.full.pdf


Estrogen exposure is a major risk factor for breast cancer. Tissue estrogen originates from the ovaries but a significant portion is also produced by enzyme activity locally in the breast itself. How these enzymes are regulated is not fully understood. The extracellular space, where the metabolic exchange and cell interactions take place, reflects the environment that surrounds the epithelium but there has been no previous study of hormone concentrations in this compartment. In the present study microdialysis was used to measure extracellular estrogen concentrations in breast tissue and abdominal subcutaneous fat in 12 healthy women in vivo. It was found that women with high plasma progesterone levels had significant increased levels of estradiol in breast tissue compared with fat tissue (breast tissue 168 6 pM; subcutaneous fat, 154 5 pM; P < 0·05), whereas women with low plasma progesterone exhibited no difference. Moreover, there was a significant correlation between local breast tissue estradiol and plasma progesterone levels (r = 0·709, P < 0·01). There was no difference in estrone sulphate in breast and fat tissue regardless of progesterone levels. Estrone was not detectable. The results in this study suggest that progesterone may be one regulator in the local conversion of estrogen precursors into potent estradiol in normal breast tissue. Journal of Endocrinology (2005) 187, 103–108

I don't get it? (Stupid blonde here)

I know this veres off what you are working on but do you think there's a definite answer to "do phytoestrogens REPLACE xenoestrogens or do phytos replace but ADD to the overall estrogen load?"

I don't get it? (Stupid blonde here)

I know this veres off what you are working on but do you think there's a definite answer to "do phytoestrogens REPLACE xenoestrogens or do phytos replace but ADD to the overall estrogen load?"

Correction, sexy blond .

Good question, I think the latter quite actually. Say (or use) this is an example, a women with a normal cycle (lol, what's that you say). She takes PM in the first half, now does her estradiol dramatically fall off after (say) day 14-16?........I think not. Calculations of blood E2 levels are still present a week if not longer. Add to this, the daily hidden barrage of xeno's (I'll bet that amount undetermined but still revelant).

Now, doe this women need to add more E in luteal?, I think not (again lol)..........and in the present study above it validates that breast tissue expression of E2 is still quite high when progesterone is added.

I don't get it? (Stupid blonde here)

I know this veres off what you are working on but do you think there's a definite answer to "do phytoestrogens REPLACE xenoestrogens or do phytos replace but ADD to the overall estrogen load?"

Correction, sexy blond .

Good question, I think the latter quite actually. Say (or use) this is an example, a women with a normal cycle (lol, what's that you say). She takes PM in the first half, now does her estradiol dramatically fall off after (say) day 14-16?........I think not. Calculations of blood E2 levels are still present a week if not longer. Add to this, the daily hidden barrage of xeno's (I'll bet that amount undetermined but still revelant).

Now, doe this women need to add more E in luteal?, I think not (again lol)..........and in the present study above it validates that breast tissue expression of E2 is still quite high when progesterone is added.

Ahh still present a week later... Ok yeh the higher E2 alongside high progesterone bit confused me too?
So it would seem it's a gamble then eh messing around with phytos even if it's just cycling if the effects can last well into luteal?.... Bugger shit and damn....

I don't get it? (Stupid blonde here)

I know this veres off what you are working on but do you think there's a definite answer to "do phytoestrogens REPLACE xenoestrogens or do phytos replace but ADD to the overall estrogen load?"

Correction, sexy blond .

Good question, I think the latter quite actually. Say (or use) this is an example, a women with a normal cycle (lol, what's that you say). She takes PM in the first half, now does her estradiol dramatically fall off after (say) day 14-16?........I think not. Calculations of blood E2 levels are still present a week if not longer. Add to this, the daily hidden barrage of xeno's (I'll bet that amount undetermined but still revelant).

Now, doe this women need to add more E in luteal?, I think not (again lol)..........and in the present study above it validates that breast tissue expression of E2 is still quite high when progesterone is added.

Ahh still present a week later... Ok yeh the higher E2 alongside high progesterone bit confused me too?
So it would seem it's a gamble then eh messing around with phytos even if it's just cycling if the effects can last well into luteal?.... Bugger shit and damn....

Bugger is right, =

Maybe NBE can be summoned up this way, women are likely to (when they do) have a slow but steady growth phase, while males seeking breast growth might have bursts of growth. Why exactly?, multiple reasons I suppose, but maybe it's narrowed down or relevant to how GH (growth hormone) is secreted in both sexes via the hypothalamus......female GH release is steady while males are in bursts.

But to your point, the extra E is not needed.