(04-05-2015, 01:12 AM)bryony Wrote: (02-05-2015, 04:44 AM)Lotus Wrote: However..........I do have an issue suggesting taking more PM is the answer, especially at 3000 mg. It's been documented increased dosages of PM/hrt (and phytoestrogens too) are ineffective.
(04-05-2015, 01:12 AM)bryony Wrote: Documented where? In the literature or anecdotally? Also, ineffective for what? Breast growth? Don't care. It certainly isn't ineffective for my GD.
I can quite categorically say that, for anxiolitic and anti-depressive effects, in my personal case, 1 gram of PM lasts about 4 hours. If today is not a bad day I can get by on 2g. If today is a bad GD day, then it could be 3,4 or 5g. That's been how I've been dealing with life for the last 3 years.
Quote:And btw, PM does carry health risks, which has been certainly documented by our BN members, (research posted on BN).
Which health risks? Anything other than vague concerns or were they positively diagnosed as related to PM? I'd certainly appreciate a reference, because I have had no problems, other than some early lower back spasms (which I now think were testicular).
Quote:I would consider taking some time off from extended use of PM, (include phytoestrogens with that statement). And that's simply because the proliferation of cancers, breast, bone, prostate. Everyone carries the cancer gene, continued stimulation of breast and other receptors increase the odds of cancers, better play it safe along the way. Adding some preventive safeguards in NBE is a smart move, we want normal growth, not malignant growth.
I'm not against playing it safe, but I've come across clinical papers that indicate a protective effect against breast cancer with PM. It certainly seems safer than Pharm E. Have you used Google Scholar for "Mirifica" and "Cancer"?
E.g.
http://www.siamnatural.com/documentation...011-09.pdf
"These preliminary results are indicative of a potential anti-cancer action of PM that may be of use in the treatment of breast cancer. Further studies are
required to confirm this possibility"
Also:
http://journal.hep.com.cn/fmd/EN/10.1007...012-0184-8
"...fairly considerable scientific researches, both in vitro in cell lines and in vivo in various species of animals including humans, have been conducted to date to address its estrogenic activity on the reproductive organs, bones, cardiovascular diseases and other climacteric related symptoms. The antioxidative capacity and antiproliferative effect on tumor cell lines have also been assessed. In general, P. mirifica could be applicable for preventing, or as a therapeutic for, the symptoms related to estrogen deficiency in menopausal women as well as in andropausal men."
In fact the preamble to the abstract of that last reference starts off:
"Pueraria mirifica is a medicinal plant endemic to Thailand. It has been used in Thai folklore medicine for its rejuvenating qualities in aged women and men for nearly one hundred years."
So if it was dangerous, you'd kind of think that the Thai authorities would know about it by now, wouldn't you? Instead, their research shows it has protective anti-cancer qualities.
However, getting back to your original comment "I do have an issue suggesting taking more PM is the answer" - let's have some context: In the case of someone experiencing sufficient GD to endanger their marriage, and contrasted with the known and proven dangers of pharmaceutical HRT (the route that a transitioner ends up with) - the real, proven dangers of breast cancer and thrombosis - I think, absolutely that a century old traditional Asian root, taken by thousands upon thousands of Thai people, where research indicates that it actually protects against cancer, then, yes, yes, yes, take as much PM as required to make your marriage work.
Because, the alternative will almost certainly be transition and the much more dangerous HRT when the GD gets bad enough, and almost certainly the end of your marriage, and definitely the end of your relationship as it was.
Over the years I've seen several people start on PM and then move on to HRT, and I conjecture it was because they saw and improvement in their mental state but not enough of an improvement, due to fears of taking more than 2g per day.
Let me state now, for the record, that I have often had 4g per day, sometimes 5g per day over the last 3 years with no ill effects, only the ability to live life like a normal human being.
Every decision in life means taking risks; I am one of the most risk-averse people that I know.
Choice 1 - take no PM - RISK: suffer GD; marriage in danger of failing
Choice 2 - go to psychiatrist and get diagnosed with extreme GD - RISK: HRT; risks of cancer and thrombosis if I don't have an orchiectomy, possible slippery slope towards an unhappy transition.
Choice 3 - take PM as needed to control GD - RISK: none that I have found documented in clinical papers as yet (but I await correction).
B.
Byrony, I like you, you a funny guy. Honestly, I like anybody that makes me laugh
. I like commentary with some flavor, I can do without the condescending of others though. I can also do without the cis-supremacy/misogyny that some seem to spam. I don't even mind someone being arrogant/pompous as long as they lace it with some self deprecation, which is you and me, ur-uhm-----us, lol. However, I don't understand the bad/cop bad/cop-----eventual good cop??, (maybe)
I wonder who wins the aurgemnets at the house of bryony??, hmm?? future reality show??, j/k
Science is so much more stimulating imo, I find compilating my GID boring, unproductive, my coping mechanism is expressed in researching solution(s) for self improvement, I find it odd that I'd take solace in PhD related science and understand it, weird....anyways, nuff about me.
My apologies OP, your thread is hopelessly hijacked, I will make this post my last in your thread, (as it pertains to bryony and me )
unless lol........it's something I totally disagree with.
bryony likes to have the last word though, which I'd be more than happy to oblige. (Never say never).
As your marriage started 1977, I was finishing high school w/plans of serving in the military. At that time I dont think I knew what a transsexual was. I lived the typical hetro/horny teenage boy life. I only found out a year later what a t/s meant, and quite by accident. I was on liberty at bar in subic bay, PI with some shipmates, we spotted another shipment who having fun with a stunning babe in the corner of bar, we were wondering wtf???, how can he be so lucky?. Well, about 5 minutes later the table goes flying up in the air and our shipment runs (all 350lbs of him) out the of the bar screaming "she's a guy, she a guy"...
Needles to say, you never saw a big man run so fast, (what am I saying, he was kid, and a mommas boy at that. poor kid.) In fact, he ran non-stop all the way back to the base, (a good 2 miles), I don't he think he took another liberty pass for about 6 months. I get not having the access to inform ourselves back then as opposed today, we are so spoiled now we all the technology at our disposal.
I also get that you're passionate about being upfront, and that's cool, (respectable). In today's day and age defining one's sexuality is much more open. Let's face, some of us who have been married ever since back in the day only had conversions of bi-curiosity/fantasy talk maybe came out in the privacy of the bedroom. Acting on those feelings were less likely at the time and only surfaced later in life, for one reason or another, shoot....a perfect example is Bruce Jenner. I recall the wheaties cereal box with Jenner on it, you would have never suspected he'd end up transitioning into a women. As I've listed there's one possible explanation of many, and maybe some are more plausible the others as opposed to my theory, but.....I prefer that theory over cowardice. A coward is desertion, deadbeats dads and other tasteless adjectives. But yes, dishonesty is taking the easy way out.....but give the guys a break, we don't know all the reasons why GID surfaces later in life, that's all I'm saying.
(04-05-2015, 01:12 AM)bryony Wrote: Documented where? In the literature or anecdotally? Also, ineffective for what? Breast growth? Don't care. It certainly isn't ineffective for my GD.
Seriously?.......hello, that's all I do is post research, in fact, of the thousands of my posts research is spread across several threads and sections. I wouldn't say something about a product or give an anecdotal without having documentation. I'll tell you what, since you were nice enough to post a couple of papers I'll make a thread with cancer exposure of phytoestrogens, PM being anti-estrogen in high doses (phytoestrogens too), and how 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) play an important role in the regulation of steroid hormones, such as estrogens and androgens. Come to think I, I already have those threads, I'll just point out the threads if you'd like.
Here's just a few,
(03-04-2015, 07:39 PM)Lotus Wrote: current research, here's an important link regarding PM. In English it might explain part of a response (growth) issue seen in genetic males. It's that gate-keeper thing (light switch) called HSD (Hydroxysteroid dehydrogenases) it's an enzyme that's positioned in-between cellular steroid hormones pathways, like E1 to E2. But science also defines them as reductase pathways.
Biological Evaluation of Deoxymiroestrol, a Potent Phytoestrogen from Pueraria candollei var. mirifica
Udomsuk L1, Putalun W1, Juengwatanatrakul T2, Jarukamjorn K1*
Introduction: Deoxymiroestrol is a phytoestrogen isolated from tuberous roots of Pueraria candollei var. mirifica (Leguminosae). Since deoxymiroestrol showed strong estrogenic-like activitiy, it is worth to investigate its biological activity on enzymes related drug metabolism, cytochrome P450s (P450), and sex hormone synthesis pathway, as well as its anti-lipid peroxidation in both in vitro in primary mouse hepatocytes and in vivo in mouse liver. Methods: P450 activities were evaluated in both primary mouse hepatocytes and mouse liver. Expression of CYP1A1, CYP1A2, CYP1B1, CYP2B9, AhR, and ARNT mRNAs were quantified by real- time RT-PCR while their activities were assessed by benzyloxyresorufin and methoxyresorufin O-dealkylation, respectively. Enzymes involved in sex-hormone synthesis pathway in male testes were semi-quantified by RT-PCR. Lipid peroxidation was measured in mouse brain. Results: In primary hepatocytes, expression of AhR, ARNT, and CYP1A1 mRNAs was suppressed whereas that of CYP1B1 was induced by deoxymiroestrol, in which the gene expressions were time- and concentration-dependent patterns compared to those of estradiol. In vivo in mice, deoxymiroestrol enlarged female uterus-weight and -volume as comparable to estradiol. As estradiol did, deoxymiroestrol induced expression of CYP2B9 mRNA whereas those of CYP1A2 were suppressed. Assessment of testicular enzymes involved in sex hormone synthesis pathway showed suppression of 3β-HSD, 17β-HSD1, and CYP17 expressions with those of CYP19 mRNA was slightly decreased by deoxymiroestrol. In addition, the expression of 17β-HSD2 was increased resulting in decreasing estradiol synthesis as that noted by estradiol. In addition, deoxymiroestrol possessed anti-lipid peroxidative activity in mouse brain. Conclusion: These observations suggested deoxymiroestrol as a potential alternative medicine for estradiol according to its distinctive abilities on regulation of related hepatic P450 enzymes and sex hormone-synthesis responsive enzymes, with its beneficent anti-oxidative potential.
http://pharm.kku.ac.th/isan-journal/jour...es_249.pdf
Ok, I think we're seeing a problem here with the down regulation of Hydroxysteroid dehydrogenases (HSDs). In paticlaur 3β-HSD, 17β-HSD1, and 17β-HSD1 catalyzes the activation of estrone (E1) to the most potent estrogen estradiol (E2), predominantly considered as an ezyme of estradiol biosynthesis. Which deoxymiroestrol seems to suppress the action, in other words in males it may interrupt the synthesis of E1 (estrone) to E2 (estradiol).
Which this theory or hypothesis lines up with PM an E1 mediator. Which Dr. Gordon commented on here, albeit from E3 to E1:
Quote:Dr Gordon: First, I have to give credit for this information to Dr. Youssef Mirhom, professor emeritus, pharmacognosist and chief scientific officer at Bio-Botanica. Estriol itself is not a hormone secreted by the ovary, but a deactivation product of estrone and estradiol in the human liver by 16-alpha-hydroxylation. Miroestrol is a phytoestrogen (a plant estrogen), and has the same chemical properties, as well as physiological properties as estriol; however, it has a weaker estrogenic effect. And Professor Sayan Sawatsri M.D., gets the credit for the following valuable bit of information—miroestrol has about 3,000 times the estrogenic activity of soy isoflavones. initially said.
Assessment of testicular enzymes involved in sex hormone synthesis pathway showed suppression of 3β-HSD, 17β-HSD1, and CYP17 expressions with those of CYP19 mRNA was slightly decreased by deoxymiroestrol. In addition, the expression of 17β-HSD2 was increased resulting in decreasing estradiol synthesis as that noted by estradiol
17β-HSD type1: 17β-HSD1 catalyzes the activation of estrone (E1) to the most potent estrogen estradiol (E2), predominantly considered as an ezyme of estradiol biosynthesis.
_________________
Hydrohysteroid Dehydrogenases –
Biological Role and Clinical Importance – Review
http://cdn.intechopen.com/pdfs-wm/40961.pdf
(20-04-2015, 11:37 PM)Lotus Wrote: Here's an interesting research paper on phytoestrogens and target tissues. The bottome line is that most phytoestrogens increase blood flow in humans (vasodilation). Interactions are important for people to understand, increasing blood flow means NOT to take anything else that increases bleeding (e.g. blood thinning agents like warfarin and others). This finding reinforces that increasing the dosages of phytoestrogens have little to no benefit. Smaller dosages of certain phytoestrogens that target certain tissues (estrogen receptor alpha-aka ER-a mammary and ER-b (beta) Bone) progesterone receptor (e.g. Vitex, FG, Progesterone cream, essential fatty acids EFA's) and NBE super foods continues to out perform PM only intake.
intakes must be above a relatively high threshold level for a lengthy period of time, and little or no extra benefit is observed with intakes above this threshold level.
phyto-oestrogens on tissues.
Anderson JJ1, Anthony M, Messina M, Garne SC.
Author information
Abstract
Recent investigations on the effects of phyto-oestrogens on various tissues have revealed that these diverse molecules may improve human health, particularly by protecting against certain chronic diseases. After a brief examination of the food sources, structures, and general cellular actions of the major phyto-oestrogens, current research findings on cardiovascular disease, skeletal tissues, and reproductive cancers are reviewed. Phyto-oestrogen concentrations in blood may be maintained at high levels in those consuming soyabean (Glycine max)-based food daily at several meals and exert their effects on target cells through either genomic effects via the classical oestrogen receptors or non-genomic effects mediated by membrane-bound oestrogen receptors or other cellular proteins. The expression of oestrogen receptor (OR) subtypes alpha (a) and beta (beta) varies across tissues, and cells that preferentially express OR-beta, which may include bone cells, are more likely to respond to phyto-oestrogens. Conversely, reproductive tissues contain relatively more OR-a and may, thus, be differently affected by phyto-oestrogens. Soyabean phyto-oestrogens appear to prevent the progression of atherosclerosis through multiple interactions, including lowering of plasma lipids and lipoproteins, increased vasodilatation and, possibly, decreased activation of blood platelets and vascular smooth muscle cells. However, a favourable impact on cardiovascular disease morbidity and mortality by a soyabean-enriched western-type diet remains to be shown, and unresolved questions remain regarding dose and form of the phyto-oestrogens in relation to risks and benefits. The isoflavones of soyabean have been shown consistently to have bone-retentive effects in animal studies by several investigators using rodent models, although intakes must be above a relatively high threshold level for a lengthy period of time, and little or no extra benefit is observed with intakes above this threshold level. The reports of modest or no effects on prevention of bone loss in human and non-human primate studies respectively, may be due to the limited doses tested so far. The relationship between soyabean-food intake and cancer risk has been more extensively investigated than for any other disease, but with less certainty about the benefits of long-term consumption of phyto-oestrogen-containing foods on prevention of cancer. The observations that breast and prostate cancer rates are lower in Asian countries, where soyabean foods are consumed at high levels, and the high isoflavone content of soyabeans have led to examination of the potential protective effects of phyto-oestrogens. Establishing diet-cancer relationships has proved difficult, in part because of the conflicting data from various studies of effects of soyabean-diets on cancer. Epidemiological evidence, though not impressive, does suggest that soyabean intake reduces breast cancer risk. The isoflavone genistein has a potent effect on breast cancer cells in vitro, and early exposure of animals to genistein has been effective in reducing later development of mammary cancer. Thus, continuous consumption of soyabean foods in early life and adulthood may help explain the low breast cancer mortality rates in Asian countries. Although the evidence for a protective effect against prostate cancer may be slightly more supportive, more research is needed before any firm conclusions can be made about the phyto-oestrogen-cancer linkages.
http://www.ncbi.nlm.nih.gov/pubmed/19087447
(05-03-2015, 05:15 AM)Lotus Wrote: This post follows up the previous information. Btw, the PDF is a complete version of the study.
(03-03-2015, 05:45 AM)Lotus Wrote: Remember these "on and off" switches?, part of this good news, the other part.....not so good.
----------------------
The good news....…
the reductase responsible for the conversion of estrone (a weak estrogen) to 17b-estradiol (a potent estrogen) is the estrogenic type 1 17b-HSD and is the `on' switch for the estrogen receptor (ER). The oxidase activities responsible for the reverse reaction and the inactivation of 17b-estradiol are the type 2 and type 4 17b-HSDs, and these function as the `off' switch for the ER.
Thus, the activity of these 17b-HSD isoforms may regulate the ligand occupancy of ERa and ERb and their trans- activation in estrogen target tissues (Wu et al., 1993; Andersson, 1995; Labrie et al., 1997; 2000).
Hydroxysteroid dehydrogenases and pre-receptor regulation of steroid hormone action http://humupd.oxfordjournals.org/content...3.full.pdf
---------------------------------
The not so good news.....
Phytoestrogens inhibit human 17b-hydroxysteroid dehydrogenase type 5
http://www.brc.dcs.gla.ac.uk/~rb106x/pub...bition.pdf
(07-02-2015, 07:37 PM)Lotus Wrote: This is a bit over simplified but Hydroxysteroid Dehydrogenases (HSDs) act like a gate-keeper just before steroids (hormones) bind to receptors (synthesis). Furthermore, these "gate-keepers" can flip the switch (a light switch) on/off to allow passage to the cell receptors. So in essence, they can inhibit or promote hormone activity. Finding a new class of HSD's is the next step, Aldo-keto reductases (AKRs) can help us get there.
(05-03-2015, 10:43 AM)spanky Wrote: Quote:The not so good news.....
Phytoestrogens inhibit human 17b-hydroxysteroid dehydrogenase type 5
http://www.brc.dcs.gla.ac.uk/~rb106x/pub...bition.pdf
That is, as they say, a real kick in the (shrinking) nuts! A "potent inhibitor" of aromatase no less! So something like PM is a direct provider of a phytoestrogen to boost breast growth, but also it defeats aromatase conversion, thus undermining breast growth from the other direction! I have been combining PM with WP for a few months, and may have been largely wasting the WP! AARRGGHH! (No, I am not a pirate.)
If that analysis is correct, then is it an either/or situation, in which you must choose your weapon but not combine them?
(10-04-2015, 05:50 AM)Lotus Wrote: (28-03-2015, 06:08 AM)Dfleurs Wrote: Hmmmm so is reishi still good to take? i guess taking everything in moderation is always better but NBE is such a long journey thus everything will be kind of long term type
Absolutely, it benefits NBE by reducing DHT and up-regulates estrogen receptors. Here's some interesting info on how estrogens behave (mayo clinic), it's been stated before that PM behave's like E1 (estrone). I've highlighted the points of interest. For example, E1 plays a role in peripheral aromatization of androstenedione (that's through the A4 pathway), IMO, it's a back door growth opportunity. But circulating E2 is the most bio-active (free) estrogen, in other words, the strongest estrogen. Phytoestrogens don't produce estrogens as we know, but they up-regulate estrogen receptors, that's where E2 (the body's own natural estrogen, not the pharma kind, that's a different topic altogether, interact with receptors and activate growth), Hopefully.
But.....if you don't reduce DHT (as we know) breast growth is very limited, that's the bottom line.....
Estrogens are involved in development and maintenance of the female phenotype, germ cell maturation, and pregnancy. They also are important for many other, nongender-specific processes, including growth, nervous system maturation, bone metabolism/remodeling, and endothelial responsiveness. The 2 major biologically active estrogens in nonpregnant humans are estrone (E1) and estradiol (E2). A third bioactive estrogen, estriol (E3), is the main pregnancy estrogen, but plays no significant role in nonpregnant women or men.
E2 is produced primarily in ovaries and testes by aromatization of testosterone. Small amounts are produced in the adrenal glands and some peripheral tissues, most notably fat. By contrast, most of the circulating E1 is derived from peripheral aromatization of androstenedione (mainly adrenal). E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25-5 times the biological potency of E1. E2 circulates at 1.5-4 times the concentration of E1 in premenopausal, nonpregnant women. E2 levels in men and postmenopausal women are much lower than in nonpregnant women, while E1 levels differ less, resulting in a reversal of the premenopausal E2:E1 ratio. E2 levels in premenopausal women fluctuate during the menstrual cycle. They are lowest during the early follicular phase. E2 levels then rise gradually until 2 to 3 days before ovulation, at which stage they start to increase much more rapidly and peak just before the ovulation-inducing luteinizing hormone/follicle stimulating hormone surge at 5 to 10 times the early follicular levels. This is followed by a modest decline during the ovulatory phase. E2 levels then increase again gradually until the midpoint of the luteal phase and thereafter decline to trough, early follicular levels.
Measurement of serum E2 forms an integral part of the assessment of reproductive function in females, including assessment of infertility, oligo-amenorrhea and menopausal status. In addition, it is widely used for monitoring ovulation induction, as well as during preparation for in vitro fertilization. For these applications E2 measurements with modestly sensitive assays suffice. However, extra sensitive E2 assays or simultaneous measurement of E1, or both are needed in a number of other clinical situations. These include inborn errors of sex steroid metabolism, disorders of puberty, estrogen deficiency in men, fracture risk assessment in menopausal women, and increasingly, therapeutic drug monitoring, either in the context of low-dose female hormone replacement therapy or antiestrogen treatment.
http://www.mayomedicallaboratories.com/t...tive/81418
Steroid Pathway
http://www.mayomedicallaboratories.com/i...thways.pdf
(23-03-2015, 04:59 AM)Lotus Wrote: (23-03-2015, 04:38 AM)Lotus Wrote: ** fatty acid synthase (FASN) in (humans)
Gene ID: 2194, updated on 21-Mar-2015
The enzyme encoded by this gene is a multifunctional protein. Its main function is to catalyze the synthesis of palmitate from acetyl-CoA and malonyl-CoA, in the presence of NADPH, into long-chain saturated fatty acids. In some cancer cell lines, this protein has been found to be fused with estrogen receptor-alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha. [provided by RefSeq, Jul 2008]
http://www.ncbi.nlm.nih.gov/gene/2194
More scientific proof that fatty acids helps with the binding process of estrogen receptor alpha (ER-a, the growth receptor). Specifically---palmitate (a solid unsaturated fat). I hope this is making sense for everybody. In other words- omega 3's and 6's needs to be in an NBE plan, the health benefits alone are worth looking into, another benefit is its ability to block DHT (e.g. Evening primrose oil, EPO).
Coconut oil
Evening primrose oil
Macadamia nut oil
Krill oil
And organic when possible.
(23-03-2015, 04:41 AM)pom19 Wrote: Thanks Lotus for this info. I really can use it. POM
Thanks Pom, I hope it helps.
(30-01-2015, 07:27 PM)Lotus Wrote: PUFA's- polyunsaturated -fats increase estrogen.
Monounsaturated-fats increase testosterone
Polyphenols (specifically Green Tea) promotes aromatase, anti-oxidation, estrogen, modifies signaling transduction pathways, relieves oxidative stress (reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance.
(09-01-2015, 09:55 PM)Lotus Wrote: Sorry for the redundancy, but in case you missed it, this is extremely important:
(08-01-2015, 06:01 AM)Lotus Wrote: Considering the potential to block DHT and increase aromatase adding fatty acids makes sense, only don't forget a fitness plan.
Anti-androgenic activity of fatty acids.
In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
(18-12-2014, 05:48 AM)Lotus Wrote: I'd say to consider the many different options out there, currently I take coconut oil, (although not a GLA) I'd consider EPO, and from what I understand you can vary (trade off) between say (borage oil, EPO, flaxseed oil or others), which FSO isn't said to contain anti-aromatase properties. But I don't mind giving T a pass through anti-aromatase while on CO, I like it, but that's just my opinion, if you don't mind smelling like a nut, it's absolutely wonderful for soft soft hair.
http://www.livestrong.com/article/441704...-primrose/
http://www.drugs.com/drug-interactions/e...10681.html
https://www.consumerlab.com/reviews/Blac.../flaxseed/
http://www.livestrong.com/article/525321...mrose-oil/
Fats and oils are essential to your health and many of your body's functions. The oils most important for brain, nerves and skin include the essential fatty acids, which are available in a variety of foods that include olive oil and avocados. Flaxseeds also provide an important essential fatty acid called omega-3, which is strongest in its oil. Evening primrose, which contains omega-6s, is not usually consumed as a food, but rather its oil is taken in supplement form.
Flaxseed oil comes from the seeds of the flax plant. This oil provides the important essential fatty acids linolenic acid and linoleic acid, according to Shawn M. Talbott in his book "The Health Professional's Guide to Dietary Supplements." Flaxseed oil contains about 57 percent linolenic acid, which is an omega-3 fatty acid, and about 17 percent linoleic acid, an omega-6 fatty acid. It is important to get a balance of omega-3 fatty acids to omega-6 fatty acids. However, the standard American diet contains too many omega-6 fatty acids and few omega-3 fatty acids. Omega-3 fatty acids help counter inflammation and increase brain function. Flaxseed oil also contains lignan, which is a phytochemical that may help cancer prevention.
Evening primrose oil comes from the herb Oenothera biennis, which has bright yellow flowers that bloom in the evening, writes Talbott. The plant grows wild in dry, arid environments, and was first documented in Britain as being used for medicinal purposes. The main oil found in evening primrose oil is gamma-linolenic acid, another essential fatty acid, though it also contains linoleic acid. People have taken evening primrose oil include to relieve PMS, hot flashes and fibrocystic breasts.
How They Differ
The main difference between flaxseed oil and evening primrose oil is that the former contains the omega-3 linolenic acid, while the latter contains the omega-6 gamma-linolenic acid, or GLA for short. Omega-3s are linked to a lower risk of heart disease, cancer and arthritis, often through their anti-inflammatory properties, notes the University of Maryland Medical Center. Though GLA is an omega-6 fatty acid, which is sometimes connected to inflammation, it is one form of omega-6 that also can reduce inflammation, but is geared more toward skin, hair, reproductive and bone health. But the University of Maryland reports that more research favors the anti-inflammatory properties of the omega-3 fatty acids found in flaxseed oil more than that of GLA found in evening primrose oil.
What to Consider
Both flaxseed oil and evening primrose oil can be healthy parts of your diet, and you can consume both at the same time. Ingesting more flaxseed oil or flaxseeds than evening primrose oil can help balance your intake of omega-3 fatty acids and omega-6 fatty acids. Possible side effects related to flaxseed oil are diarrhea if you consume large amounts and the increased risk of bleeding if you suffer from a bleeding disorder. Nausea, upset stomach or diarrhea may occur if you take too much evening primrose oil.
Oh I almost forgot,
Side Effects of PM (BN members)
http://www.breastnexus.com/showthread.php?tid=22977