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Fenugreek increases estradiol

#11

You're welcome , and thank you for the lovely comments. If you'd like an NBE/HrT topic researched (time permitting) I'll do my best to fill in the blanks or hopefully make sense of what the science is saying, (from a noob interpretation that is, lol).

eh, if we learn something along the way??, Blush hopefully it helps someone, fwiw. Smile.
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#12

(06-05-2016, 05:01)Lotus Wrote:  You're welcome , and thank you for the lovely comments. If you'd like an NBE/HrT topic researched (time permitting) I'll do my best to fill in the blanks or hopefully make sense of what the science is saying, (from a noob interpretation that is, lol).

eh, if we learn something along the way??, Blush hopefully it helps someone, fwiw. Smile.

Thank you so much for doing what you do . . .
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#13

(28-04-2016, 05:21)Lotus Wrote:  I wouldn't take FG all cycle tbh, I mean why would you?. Perhaps in luteal would make more sense for the ladies. For male breast growth maybe 1x per day, (mid-day?) and 2 weeks out of the month. The reason I think relates to hormonal out-put, and from the study only 300 mg was used to influence the upregulation.

Lotus, So now that you have taken fenugreek off the table, what do you recommend to increase prolactin?
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#14

(06-05-2016, 16:31)Highhope Wrote:  
(28-04-2016, 05:21)Lotus Wrote:  I wouldn't take FG all cycle tbh, I mean why would you?. Perhaps in luteal would make more sense for the ladies. For male breast growth maybe 1x per day, (mid-day?) and 2 weeks out of the month. The reason I think relates to hormonal out-put, and from the study only 300 mg was used to influence the upregulation.

Lotus, So now that you have taken fenugreek off the table, what do you recommend to increase prolactin?

I don't know what Lotus thinks, but from my own research Shatavari is the only herb with proven efficacy and wide availability.
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#15

Thanks stevenator. Wink

FG is still on the table, I'm not excluding it, just when to take it. Also, find a a standerized version of FG (over 50% saponins). Agree with Abi I do, Wink shatavari is versatile, so is FG (both will raise PRL).

Raising prolactin means lowering (inhibiting) dopamine, specifically @ the inhibition of D2 receptors:

Conventional antipsychotic agents and some, but not all, of the marketed novel agents, elevate serum prolactin levels via inhibition of dopamine action at receptors in the tuberoinfundibular system of hypothalamus, where prolactin secretion is regulated. Specifically, the neurotransmitter dopamine, which acts as the primary prolactin inhibiting factor, is provided to the pituitary gland by the dopaminergic neurons of the periventricular and arcuate nuclei of the medial basal hypothalamus, through the pituitary venus system [1, 9, 10]. Dopamine stimulates receptors located on the surface of the lactotroph pituitary cells and provokes a tonic suppression on prolactin secretion. On the other hand, serotonin stimulates prolactin release [5, 9, 11]. In addition, neuropeptides such as thyrotropin releasing hormone TRH, oxytocin, vasoactive intestinal polypeptide VIP, and peptide histidine-methionine, which are under the control of serotonin, promote prolactin (PRL) secretion.
http://www.hindawi.com/journals/schizort/2013/502697/


Fenugreek raises prolactin, so does anti-psychotics, vitamin B5, gluten (yes gluten), soy products.


Vitamin B5
https://www.healthaliciousness.com/artic...min-B5.php


Gluten exorphin B5 stimulates prolactin secretion through opioid receptors located outside the blood-brain barrier.


Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response.[4][5] Some block activation of all types of β-adrenergic receptors and others are selective for one of the three known types of beta receptors, designated β1, β2 and β3 receptors.[6] β1-adrenergic receptors are located mainly in the heart and in the kidneys.[5] β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.[5] β3-adrenergic receptors are located in fat cells.[7]

Sorry, I'll post more asap. Big Grin
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#16

It's interesting what melatonin does to prolactin, (daytime supplementation reacts the same as nighttime).

Role of melatonin in nocturnal prolactin secretion in women with normoprolactinemia and mild hyperprolactinemia.
Okatani Y, et al. Am J Obstet Gynecol. 1993.
Show full citation
Abstract
OBJECTIVE: Our objective was to clarify the relationship between the nocturnal melatonin surge and the nocturnal prolactin release in women with normoprolactinemia and mild hyperprolactinemia.

STUDY DESIGN: Nocturnal serum melatonin and prolactin levels were determined for a various awake/sleep and light/dark conditions in a total of 23 healthy normoprolactinemia and 9 mild hyperprolactinemia. Patterns of prolactin and melatonin levels were subject to analysis of variance.

RESULTS: During sleep deprivation under continuous illumination in normoprolactinemia, neither melatonin nor prolactin increased in concentration. In contrast, during sleep deprivation in a dark environment, both hormones were increased. The maximal prolactin levels in mild hyperprolactinemia under physiologic sleep/dark were significantly higher (p < 0.01) and were reached 2 hours earlier than in normoprolactinemia. However, each woman with mild hyperprolactinemia had similar melatonin surges. Oral administration (1 mg) of melatonin to normoprolactinemia and mild hyperprolactinemia in the daytime resulted in release of prolactin in a fashion similar to that observed during the night.

CONCLUSION: Melatonin can regulate nocturnal prolactin secretion independent of sleep-related factors. Furthermore, the nature of the response to exogenous melatonin administration suggests that mild hyperprolactinemia may be unusually sensitive to melatonin.

PMID 8456892 [PubMed - indexed for MEDLINE
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#17

You inbox is full Smile - cant escape me that easy...
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#18

Hey Lotus Smile
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)
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#19

(01-08-2016, 15:04)missboobshirt Wrote:  Hey Lotus Smile
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, Smile

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).

Quote: 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 (lutenizing hormone @ 41%)......thus the need for additional 5 AR inhibitor.

To me, FG needs to be in first half and Vitex in the second half. I'll have to adjust the supplement info about FG lowering progesterone. Alternately, 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 albilty in EGF (epidermal growth factor), I'll post more info on the X thread.

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

Smile
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#20

Oh no Sad I definitely don't want something that lowers progesterone. I guess I will have to re think my desire to try FG :/ Maybe some time in the future I will come around again and ask you about FSO or Hops Oil :p Thanks so much for all this info Lotus <3 you're the best.
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