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Project X (hrt)

Here's the puresterol data... assays are included
http://www.bio-botanica.com/articles/Pue...folder.pdf

20 mg miroestrol and 20 mg isoflavone per 100 gm (2% !?)

My latest experimental idea is using DMSO as a solvent/delivery system for topical herbal application. DMSO has a bad rap in the US... worst thing about it is containing it, and the affect on body odor. This looks promising as a base:
http://www.naturalhealthyconcepts.com/dm...fgod2-IAhg

Not sure I'm going to follow through, but I think a DHEA and/or PM powder dissolved in DMSO could work, when combined with DMSOs benefits (supposedly potentiates what it delivers).

Warning to anyone trying it: DMSO will take just about anything into your blood stream.... including what's on your skin where applied. Most lotions have things in them that don't belong in your bloodstream.

-j
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(24-03-2016, 04:46 AM)Fire And Ice Wrote:  I don't maybe you're onto something, after all the brain is the most erogenous zone. Stupid perverted brain. Blush Tongue


Lol, there's something going on fo sure. RolleyesSmile

(24-03-2016, 05:01 AM)iaboy Wrote:  Thank God the noise I heard was you sucking up to Eve.... There for a bit, I thought it was a horse pulling a hoof out of mud. hehehe..

Oh well, whatever it takes, right Lotus?TongueBig Grin

PPPPPPPPPPPPfffffffffffffffffttttttttttttttttttt!!!! Big Grin
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(24-03-2016, 05:53 AM)jamixoxo Wrote:  Here's the puresterol data... assays are included
http://www.bio-botanica.com/articles/Pue...folder.pdf

20 mg miroestrol and 20 mg isoflavone per 100 gm (2% !?)

My latest experimental idea is using DMSO as a solvent/delivery system for topical herbal application. DMSO has a bad rap in the US... worst thing about it is containing it, and the affect on body odor. This looks promising as a base:
http://www.naturalhealthyconcepts.com/dm...fgod2-IAhg

Not sure I'm going to follow through, but I think a DHEA and/or PM powder dissolved in DMSO could work, when combined with DMSOs benefits (supposedly potentiates what it delivers).

Warning to anyone trying it: DMSO will take just about anything into your blood stream.... including what's on your skin where applied. Most lotions have things in them that don't belong in your bloodstream.

-j

Thanks Jamie,

...... that's interesting, thanks for the links. Is purestrol your current brand of PM?. DHEA is interesting, meaning what it can do in the highly estrogenic state expressed in older men, either on NBE/Hrt. I think its ability for interconversion should only be used by experienced users, such as yourself. I've tried a tincture of transdermal DHEA to the breasts, I felt it was a similar response as PC, though that's just me.

Good luck, please keep in touch with the results. Smile
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[attachment=11687]An update since?, sorry I can't remember lol. Blush these pictures are taken laying on my back. (1st time stacking pics though).
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Lotus, you apparently made claims somewhere that fish oil raises DHT, I am wondering what academic sources you had for that if any?
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(24-03-2016, 08:53 PM)AbiDrew85 Wrote:  Lotus, you apparently made claims somewhere that fish oil raises DHT, I am wondering what academic sources you had for that if any?

You are funny, " academics sources if any ".........(sources are listed in the endocrine section), listed below though. Knowing more about how negative feedback works can help get to new places of discovery.


(26-06-2015, 08:49 AM)Lotus Wrote:  
(26-06-2015, 07:38 AM)bobie Wrote:  Just an omega 3, this is the one http://opti3omega.com/ but since im due to run out soon i wondered whether a combi would be better, thanks


I found out my fish oil supplement had triglycerides, which is what I thought I was avoiding. In fish oil the EPA and DHA are mainly bound to triglycerides, while in krill oil fatty acids are bound to phospholipids.

Phospholipids are important components of all cell membranes. They are also involved in some cellular signaling pathways, the molecular method cells use to telegraph information about physiological changes in their environments. Fatty acids, in addition to being components of phospholipids, are also involved in the storage of excess energy in fats known as tricylglycerols.
http://www.wellwise.org/blogs/charles-sp...atty-acids

So if you're looking into a new omega 3, look into krill oil, here's some more info on it. But I definitely believe lipid metabolism plays a big role in fatty acid synthesize of hormones, plus many other functions including diabetes, androgens (lowering), aromatase, aids in depression and so many other things.

(I'm not suggesting this supplement, I list it because it's great material with referenced study's).
SUPERBA KRILL POWDER
http://www.superbakrill.com/wp-content/u...-Paper.pdf


Alteration of the lipid composition of rat testicular plasma membranes by dietary (n-3) fatty acids changes the responsiveness of Leydig cells and testosterone synthesis.
Sebokova E1, Garg ML, Wierzbicki A, Thomson AB, Clandinin MT.
Author information
Abstract
Experiments were conducted to assess whether changing dietary fat composition altered phospholipid composition of rat testicular plasma membranes in a manner that altered receptor-mediated action of luteinizing hormone (LH)/human chorionic gonadotropin (hCG). Weanling rats were fed diets that provided high or low cholesterol intakes and that were enriched with linseed oil, fish oil or beef tallow for 4 wk. Feeding diets high in (n-3) fatty acids decreased plasma and testicular plasma membrane 20:4(n-6) content. A marked reduction of the 22:5(n-6) content and an increase in the 22:6(n-3) content of testicular plasma membrane was found only in animals fed fish oil. A decrease in binding capacity of the gonadotropin (LH/hCG) receptor in the plasma membrane, with no change in receptor affinity, was observed for animals fed either linseed oil or fish oil diets. Dietary treatments that raised plasma membrane cholesterol content and the cholesterol to phospholipid ratio in the membrane were associated with increased binding capacity of the gonadotropin receptor. Feeding diets high in 18:3(n-3) vs. those high in fish oil altered receptor-mediated adenylate cyclase activity in a manner that depended on the level of dietary cholesterol. Feeding diets high in cholesterol or fish oil increased basal and LH-stimulated testosterone synthesis relative to that in animals fed the low cholesterol diet containing linseed oil. It is concluded that changing the fat composition of the diet alters the phospholipid composition of rat testicular plasma membranes and that this change in composition influences membrane-mediated unmasking of gonadotropin receptor-mediated action in testicular tissue.

(25-03-2015, 01:33 AM)Lotus Wrote:  Hi Clelia, (my scientist friend).

It's nice to hear from you again, it's truly an honor and inspiration hearing your comments, it takes my breath away. Tbh, when I research the reward is finding anything that remotely benefits breast growth and overall health. Blush Time after time science/research continually takes my breath away. It's like finding your first love Rolleyes, albeit in an abstract lol.....(does that sound craZy?) lol.......ok, that's probably over the top, but it's something in that order. Im my case your never to old to rediscover our potential......Big GrinTongue

(24-03-2015, 11:15 PM)-Clelia- Wrote:  Finally, could you help me? I'm looking information for "bad estrogen" that make growth faster

Sure, my pleasure.....

Those E metabolites are 16α-OH estrone & 2-OH estrone, I list this study below from 2008, it's pretty interesting, the findings are different from what I've seen.

[These data do not support the hypothesized inverse associations with 2-OH estrone and the 2:16α-OH estrone ratio nor the hypothesized positive association with 16α-OH estrone].

Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast cancer among postmenopausal women
----------------------
Abstract

Circulating estrogens are associated with breast cancer risk in postmenopausal women. Given that estrogen metabolites are potentially both mitogenic and genotoxic, it is possible that plasma levels of estrogen metabolites are related to breast cancer risk. We conducted a prospective, nested case- control study within the Nurses' Health Study. Blood samples, collected in 1989-1990, were assayed for 2-OH estrone and 16α-OH estrone among 340 cases and 677 matched controls not taking postmenopausal hormones. Multivariate relative risks (RR) and 95% confidence intervals (CI) were calculated by conditional logistic regression, adjusting for breast cancer risk factors. Neither 2-OH estrone nor 16α-OH estrone concentrations were significantly associated with breast cancer risk overall (top vs. bottom quartile RR=1.19, 95% CI (0.80-1.79), p-trend=0.40 for 2-OH estrone and RR=1.04, 95% CI (0.71-1.53), p-trend=0.81 for 16α-OH estrone). The ratio between the two metabolites (2:16α-OH estrone) was similarly unrelated to risk overall (1.30, 95% CI (0.87-1.95), p- trend=0.35). While no associations were detected among women with ER+/PR+ tumors, significant positive associations were observed for 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors (2-OH estrone RR=3.65 95% CI (1.23-10.81), p-trend=0.01, p- heterogeneity=0.02; 2:16α-OH estrone RR=3.70, 95% CI (1.24-11.09), p-trend=0.004, p- heterogeneity=0.005). These data do not support the hypothesized inverse associations with 2-OH estrone and the 2:16α-OH estrone ratio nor the hypothesized positive association with 16α-OH estrone. The significant positive associations with 2-OH estrone and the 2:16 OH estrone ratio among women with ER-/PR- tumors needs to be replicated in future studies.

http://www.ncbi.nlm.nih.gov/pmc/articles...s52956.pdf
___________________________________

The following is model I'm trying to complete in my mind, Rolleyes

For instance--hormones diffuse across membranes, are ion channels the entry point??, ERE, ER, AR, PR exist in the same cell, can carrier proteins distinguish a preferential binding?, Dexamethasone is an aromatase, Palmitate is proteins in ER-a, assuming FA's can muscle their way into the cytoplasm, from there transcription?........


Lipoxygenases (EC 1.13.11.-) are a family of iron-containing enzymesthat catalyze the dioxygenation of polyunsaturated fatty acids in lipidscontaining a cis,cis-1,4- pentadiene structure. It catalyses the following reaction:

fatty acid + O2 = fatty acid hydroperoxide

Lipoxygenases are found in plants, animals and fungi. Products of lipoxygenases are involved in diverse cell functions.

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

Quote:.[2] In mammals a number of lipoxygenases isozymes are involved in the metabolism of eicosanoids(such as prostaglandins, leukotrienes and nonclassic eicosanoids).[3] Sequence data is available for the following lipoxygenases:


compounds attack cell membranes and red blood cells, and they even cause damage to DNA and RNA strands, leading to cellular mutations in the body’s tissues. In skin, it causes wrinkles and premature aging. In blood vessels, the buildup of plaque. In tissues and organs, it can set the stage for tumors to form. I think you get the picture. Free radicals are bad, bad news, and they’re ever-present in industrial PUFA oils.
-----------------------

On a different note......

The TG (triglyceride) form of fish oil contains its own monoglyceride substrate; whereas EE fish oils, coupled to ethanol, do not. EE must therefore obtain a glycerol substrate from another source. Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Furthermore, this delay of TG re-synthesis in EE fish oils could cause an increase in free fatty acids and subsequent oxidation of those free fatty acids.

I'm gonna out on on limb here.....,I wonder if ethanol release stated below could be in part what converts to aromatase.

During the digestive process, EEs are converted back to TGs by intestinal enterocytes1 which, results in the release of ethanol. Although the amount of ethanol released in a typical dose of fish oil is small, those with sensitivities to alcohol or those who are alcoholics should refrain from the consumption of EEs.

Fish Oil Triglycerides vs. Ethyl Esters: A comparative review of absorption, stability and safety concerns
http://pi-bill-articles.blogspot.com/201...s.html?m=1




In vitro study: fish oil is anti-estrogenic

High doses of the fish fatty acid DHA may help protect the body from the impact of the female sex hormone estradiol. This is suggested by research done at the National Taiwan University, in which molecular scientists exposed human breast cancer cells to the fatty acid in test tubes. The experiment showed that DHA encourages cells to break down estradiol receptors.


Thursday, June 6, 2013
Fish Oil Triglycerides vs. Ethyl Esters: A comparative review of absorption, stability and safety concerns

http://pi-bill-articles.blogspot.com/201...s.html?m=1


Incorporation of n-3 fatty acids into plasma lipid fractions, and erythrocyte membranes and platelets during dietary supplementation with fish, fish oil, and docosahexaenoic acid-rich oil among healthy young men.
Vidgren HM1, Agren JJ, Schwab U, Rissanen T, Hänninen O, Uusitupa MI.
Author information


Abstract
The effects of n-3 fatty acid supplementation in the form of fresh fish, fish oil, and docosahexaenoic acid (DHA) oil on the fatty acid composition of plasma lipid fractions, and platelets and erythrocyte membranes of young healthy male students were examined. Altogether 59 subjects (aged 19-32 yr, body mass index 16.8-31.3 kg/m2) were randomized into the following diet groups: (i) control group; (ii) fish diet group eating fish meals five times per week [0.38 +/- 0.04 g elcosapentaenoic acid (EPA) and 0.67 +/- 0.09 g DHA per day]; (iii) DHA oil group taking algae-derived DHA oil capsules (1.68 g/d DHA in triglyceride form); and (iv) fish oil group (1.33 g EPA and 0.95 g DHA/d as free fatty acids) for 14 wk. The fatty acid composition of plasma lipids, platelets, and erythrocyte membranes was analyzed by gas chromatography. The subjects kept 4-d food records four times during the study to estimate the intake of nutrients. In the fish diet, in DHA oil, and in fish oil groups, the amounts of n-3 fatty acids increased and those of n-6 fatty acids decreased significantly in plasma lipid fractions and in platelets and erythrocyte membranes. A positive relationship was shown between the total n-3 polyunsaturated fatty acids (PUFA) and EPA and DHA intake and the increase in total n-3 PUFA and EPA and DHA in all lipid fractions analyzed. DHA was preferentially incorporated into phospholipid (PL) and triglyceride (TG) and there was very little uptake in cholesterol ester (CE), while EPA was preferentially incorporated into PL. and CE. The proportion of EPA in plasma lipids and platelets and erythrocyte membranes increased also by DHA supplementation, and the proportion of linoleic acid increased in platelets and erythrocyte membranes in the DHA oil group as well. These results suggest retroconversion of DHA to EPA and that DHA also interferes with linoleic acid metabolism.


Exercise training-induced triglyceride lowering negatively correlates with DHEA levels in men with type 2 diabetes
http://www.nature.com/ijo/journal/v25/n8...1637a.html
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Thank you, I could not seem to find your sources nor could anyone else. That's all I needed.

So it seems to be related to two things, first: triglyceride form only, second: high dose dependence. I doubt then my fairly low dose used for synergy with EGCg would be much problem even if it was triglyceride form, and, indeed, has not seemed to be, I was actually getting pretty fast response towards both my stated goals, too bad I got hit by side effects of liver damage. I also just double checked my label and the oil is sourced from sardine and anchovies and processed to ethyl ester form, so it'd actually have the possible estrogenic effect if anything. Btw, even at doses up to 2 grams, I've not had any such effect on this supplement by itself... Only in synergistic combo with EGCg to improve the latters absorption, which means the estrogenic benefits came entirely from the EGCg.

Unfortunately, from your research it seems I was also worsening the liver damage from the combo due to the fish oil being EE. I can't not finish using what I have, but will definitely be considering that before my next purchase.

Thanks again for answering me. There's a lot here as you well know and can be hard to find even for us vets.

Ugh. You have no idea how hard this is to do on this damned iPad that always wants to replace my complex words with total gibberish, so if any of this seems short, that's why.
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Cholesterol is the precursor (for all hormones) that converts testosterone (via the leydig cells,) which sigals the lutenizing hormone ------to either produce more or less T, other factors regulate this process too though. These formulated esters can be tanking NBE imo and we don't even know yet. (Yikes)

For the non geek types it might be easier to see T explained from this publication:

how testosterone is made
http://www.artofmanliness.com/2013/01/15...e-is-made/

Note: referenced under " where and how testosterone is made " no. 4
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Abi, no sweat Rolleyes,

as you know, you da bomb. RolleyesBig Grin I do reach for Fish Oil when I reach the cellar of T production (depression) a 1000 mg capsule maybe (2) helps, though it takes a few days. And there's always the T surge you get when we start messing with LH supplements, then usually should level out.

Smile
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#crying!!

Lotus I love your update piccies I come to your thread just to see them!! I love the shape you have, I always was very keen to that shape I think it's cute!! Big Grin want that symmetry!
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