[Lotus]

Great idea having a subforum for PCOS, thank you Eve and to the person?
who suggested it.

Here's a collection of posts covering PCOS over the years I've posted. I have additional info on PCOS I'll add asap.

Here's a simpler way to look at PCOS in my opinion. Sometimes SHBG has too much androgens in the bloodstream, and they happen to be "free androgens".

In other words, as quoted in science: 
"Low SHBG levels result in a sustained increase in the circulating free androgen concentration"... which can turn into DHT and subsequently create PCOS (polycystic ovarian syndrome).

So the goal for all PCOS sufferers is to "RAISE SHBG Levels"....not lower it. And when you raise SHBG you slowly turn off PCOS. That's my viewpoint. Start finding ingredients and things that increase SHBG. 

What raises SHBG?..One study below indicates vitamin D3 between 1,000iu to 4,000iu per day raises SHBG and has a beneficial effect on lowering androgens.

• Metformin raises SHBG, but it's really hard on digestion
  

• Drinking coffee can raise SHBG
  

Effects of vitamin D supplementation in women with polycystic ovary syndrome: a review

Daniela Menichini et al. Gynecol Endocrinol. 2020 Jan.
Abstract

Increasing evidence supports the contribution of vitamin D deficiency (VDD) in metabolic disturbances among women with polycystic ovary syndrome (PCOS). This review aims to assess the associations between vitamin D levels and metabolic/endocrine dysregulations and to determine the effects of vitamin D supplementation on glucose metabolism, insulin sensitivity, lipid profile, and hormone functionality in PCOS patients. We searched in PubMed human randomized controlled trials (RCTs) published in English between 2016 and 2019 on the effects of vitamin D supplementation on PCOS. Nine studies were included and analyzed. Vitamin D supplementation restored physiological serum 25(OH)D levels in PCOS women in all the studies included. In six studies, it significantly decreased fasting plasma glucose and brought improvements in insulin resistance (IR) and serum fasting insulin. In addition, four studies reported decreases of serum triglycerides, while discordant data are reported as far as LDL, HDL, and total cholesterol levels. High-doses of vitamin D (4000 IU), compared with low-dose (1000 IU), and placebo, showed beneficial effects on total testosterone, sex hormone-binding globulin (SHBG) and free androgen index (FAI). Vvitamin D supplementation at high doses for a period of at least 12 weeks, may lead to improvement in terms of glucose level, insulin sensitivity, hyperlipidemia, and hormonal functionality in PCOS women.

Effect of Long-Term Treatment with Metformin Added to Hypocaloric Diet on Body Composition, Fat Distribution, and Androgen and Insulin Levels in Abdominally Obese Women with and without the Polycystic Ovary Syndrome 
https://academic.oup.com/jcem/article/85/8/2767/2852497

It's reported that 88% of women with PCOS are related to insulin resistance (IR), and of the 12% it'll be from adrenal issues. 

Metformin lowers the insulin response (or insulin resistance), meaning lowering blood glucose. 

But let's back things up for a minute and start with stomach acid. See, if PCOS dysfunction can be controlled it needs to start with inhibiting stomach gastrin, then raise SHBG.

Metformin has side effects of nausea, diarrhea, flatulence, bloating, anorexia, metallic taste and abdominal pain. 

Metformin stimulates AMP-activated protein kinase (AMPK) and is also referred to as the master regulator of energy homeostasis. There is however a conflict with metformin as it inhibits aromatase (via AMPK production), meaning it inhibits breast growth.

Role of metformin in the management of polycystic ovary syndrome
https://www.ncbi.nlm.nih.gov/pmc/article...o=0.602410
I refer to metformin here because of its action, lowering insulin. 

Reducing inflammation can start in the mitochondria, which is its place of origin...aka-Mitochondrial Dysfunction.

Mitochondrial Dysfunction and Damage Associated Molecular Patterns (DAMPs) in Chronic Inflammatory Diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5988941

I posted information regarding how inhibiting stomach gastrin helps breast growth, but the information on inhibiting gastrin follows the same hypothesis of treating PCOS by inhibiting gastrin.

https://www.breastnexus.com/showthread.php?tid=22417&pid=207918&highlight=inflammation#pid207918

Good luck.
L.

Vitamin D3 may indirectly affect cAMP production from PGE1 by 5x, in other words, this (D3) will help upregulate aromatase. 

1,25 DIHYDROXYCHOLECALCIFEROL INDUCES AN INCREASE IN PGE 1 - AND FORSKOLIN-STIMULATED CYCLIC AMP PRODUCTION IN T47D HUMAN BREAST CANCER CELL LINE
ABSTRACT — The effect of 1, 25-dihydroxycholecalciferol [1, 25(OH)2 D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2 D3 markedly inhibited proliferation of T47D cells in a time- and concentration-dependent manner. 1,25(OH)2 D3 5 times 10−7 reduced to 70% [3H]thymidine incorporation into DNA. Specific high affinity nuclear receptors for 1,25(OH)2 D3 were present in this cell line. The cAMP produced by T47D cells was measured during 10 min stimulation by effectors (prostaglandin E1 or forskolin). Without effector, T47D cells produced similar amounts of cAMP in control and 1,25(OH)2 D3-treated cells. After 3 days in the presence of 1,25(OH)2 D3, cAMP production was significantly increased compared to control cells when stimulated by 10−4 M prostaglandin E1 or 5 times 10−7 M forskolin (3.2- and 2.4-fold increase, respectively). This cAMP increase was concentration dependent within the same range that inhibited cell growth and clonogenicity. These results suggest that 1,25(OH)2 D3 may indirectly affect cAMP production by modulating the target cell response to stimulatory agents of cAMP production.
http://www.researchgate.net/publication/..._CELL_LINE

Vitamin D analogs significantly upregulated E2- and DHT-induced CK response. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs). An estrogenic response (from vitamin D) is seen in the intestinal tract. Vitamin D also helps with hair growth.

Interaction Between Estrogen and Vitamin D–Endocrine System: A Potential Addition to the Unitary Model of Osteoporosis
http://onlinelibrary.wiley.com/doi/10.13....1954/full

Vitamin D modulation of the activity of estrogenic compounds in bone cells in vitro and in vivo.
Somjen D1.
Author information
Abstract
Vitamin D analogs modulate different organs, including modulation of energy metabolism, through the induction of creatine kinase (CK) activity. Skeletal organs from vitamin D-depleted rats showed lower constituent CK than those from vitamin D-replete rats. Moreover, estradiol-17beta (E2) or dihydrotestosterone (DHT), which increased CK in organs from intact female or male rats, respectively, stimulated much less CK in vitamin D-depleted rats. Treatment of intact female rats with non calcemic vitamin D analogs significantly upregulated E2- and DHT-induced CKresponse. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs) in organs from intact or ovariectomized (Ovx) female rats but abolished SERMs' inhibitory effect on E2-induced CK. These analogs significantly increased estradiol receptor alpha (ERalpha) protein in skeletal organs as well as histomorphological and biochemical changes due to this treatment followed by E2 or DHT. The analogs alone markedly altered the growth plate and the trabeculae and increased trabecular bone volume (%TB V) and trabecular width. The addition of E2 or DHT to this treatment restored all parameters as well as increased %TBV and cell proliferation. Treatment of Ovx female rats with JK 1624 F2-2 (JKF) decreased growth-plate width and increased %TB V, whereas QW1624 F2-2 (QW) restored growth-plate width and %TB V. Treatment of E2 with JKF restored %TBV and growth-plate width, whereas E2 with QW restored all parameters, including cortical width. There was also upregulation of the response of CK to E2 in both combined treatments. Our human-derived osteoblast (hObs)-like cell cultures respond to estrogenic compounds, and pre-treating them with JKF upregulated the CK response to E2, raloxifene (Ral), and some phytoestrogens. ERalpha and ERbeta proteins, as well as mRNA, were modulated by CB 1093 (CB) and JKF. JKF increased specific nuclear E2 binding in female hObs but inhibited specific membranal E2 binding. hObs express 25 hydroxyvitamin D3-1alpha hydroxylase (1-OHase)-mRNA and its biological activity, which are both modulated by parathyroid hormone (PTH) and estrogenic compounds. Our results demonstrate mutual interaction between vitamin D and estrogenic compounds. We therefore conclude that combined treatment with less-calcemic analogs of vitamin D and estrogenic compounds might be superior for treatment of bone damage caused by ovariectomy in female rats, with possible application for postmenopausal osteoporosis.
PMID: 17725484 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/17725484

Flaxseed oil can be antiestrogenic for some people, saw palmetto inhibits progesterone receptors and reduces estrogen. So I'd eliminate flaxseed and Saw Palmetto, instead opting for GTE (green tea extract), which new research shows GTE inhibits Sirt1 (Sirtuins) which is a known longevity pathway (extending life span). 

Flaxseed (lignans) anti-estrogenic https://www.breastnexus.com/showthread.php?tid=20403 

Saw Palmetto #1 w/o Theory
https://www.breastnexus.com/showthread.php?tid=17712&pid=97596#pid97596

The plant steroids in saw palmetto act on progesterone receptors, an action that causes a reduction in estrogen levels. According to the results of a large international trial published in the "Journal of Clinical Oncology" in April 2011, estrogen and progesterone receptor status is a predictive marker of early breast cancer and post-treatment relapse.
https://www.medicinenet.com/saw_palmetto...tamins.htm
http://www.drugs-forum.com/forum/showthread.php?t=97842#ixzz2rExiZdx7

Inhibit DHT in the liver. (reishi inhibits serum DHT @ 80%) dutas @93%, finasteride @70% and saw palmetto inhibits DHT @ 32%, in other words reishi is a stronger anti-androgen over daw Saw Palmetto.

Technically, MSM stimulates the stat5 pathway which facilitates phosphorylation and the nuclear translocation and DNA binding...in other words it helps with breast growth. MSM also stimulates prolactin and enhances GH (growth hormone)...but it needs to be taken in certain amounts... 3grams.

Some women who have pcos don't even know it. In the literature below describes DHEA-S is actually lowered overtime. The study is quite interesting because it describes some of the symptoms of PCOS.

DHEA and polycystic ovarian syndrome: Meta-analysis of case-control studies
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8691613/

PCOS women tend to suffer from psychological symptoms of mood swings, depression and anxiety, I'm listing a few of the highlights from the Meta-analysis. Some fit some don't.

It is known that acute psychosocial stress increases cortisol release in response to ACTH. As, dehydroepiandrosterone (DHEA) and its sulphated form (DHEA-S) are also released from adrenals in response to ACTH, it is quite logical to regard that the DHEA is also increased in response to acute stress [11]. However, long term psychosocial stress causes a decline in the levels of DHEA and its sulphated form, as it plays a role in resilience and successful adaptation to extreme stress [12].

30 studies were qualified for meta-analysis. Three studies were further separated as they had more than one case-control group. Therefore, the total number of final studies included was 33 articles.

PCOS women with infertility tend to be more anxious and this often sparks into a vicious cycle where increased anxiety and stress worsens infertility and vice-versa. Moreover, these women tend to adopt unhealthy eating behaviors and sedentary lifestyle so as to cope up with the psychological distress and emotional trauma.

Happy New Year my dear Lotus!

So, 500mg of Green Tea would benefit PCOS ? 

Hi Sweets, it's gotta have EGCG at least 45% to benefit pcos and breast growth. I use it and it does wonders for my hrt program. 

I'm concerned with adding fenugreek knowing it is lowering SHBG now, which goes in the opposite direction of reducing PCOS (we want to increase SHBG in PCOS). Fenugreek is great for reducing blood sugar, insulin resistance and other good things. Maybe there's a counter trade off by adding more protein to offset the difference?...I don't know, you'd have to experiment if you're comfortable doing so, or just hold off on the Fenugreek till later and be patient. 
Sex hormone-binding globulin and polycystic ovary syndromehttps://www.sciencedirect.com/science/ar...via%3Dihub

Progesterone lowers SHBG too, so... I'm looking into whether this presents an issue or not.

I'm concerned with adding fenugreek knowing it is lowering SHBG now, which goes in the opposite direction of reducing PCOS (we want to increase SHBG in PCOS). Fenugreek is great for reducing blood sugar, insulin resistance and other good things. Maybe there's a counter trade off by adding more protein to offset the difference?...I don't know, you'd have to experiment if you're comfortable doing so, or just hold off on the Fenugreek till later and be patient (which is advisable). 

Sex hormone-binding globulin and polycystic ovary syndrome
https://www.sciencedirect.com/science/ar...via%3Dihub