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PCOS and RPB4
From what I understand, there’s some connection between Polycystic Ovarian Syndrome and elevated Retinol Binding Protein 4 (the form of RBP in the plasma) levels.
I haven’t read the studies (it’ll take me days to do so for various reasons—I’m also not the best person to interoperate these anyway, since I’m not a scientist and I have to look up a lot of words along the way 😆), but thought I would post links to some of them (titles in bold above links, quotes below in italics):
Association between retinol-binding protein 4 and polycystic ovary syndrome: A meta-analysis
https://www.jstage.jst.go.jp/article/endocrj/61/10/61_EJ14-0186/_article
“Our meta-analysis results indicated that RBP4 might be a useful tool for identifying PCOS women.“
Retinoids and retinol differentially regulate steroid biosynthesis in ovarian theca cells isolated from normal cycling women and women with polycystic ovary syndrome.
https://academic.oup.com/jcem/article/90/8/4858/2838533
“The differential response of CYP17, CYP11A1, and STAR gene expression to retinoids in normal and PCOS theca cells further suggest that PCOS cells may have intrinsic differences in their ability to respond to retinoids as well as synthesize retinoids. Therefore, it is possible that stimulation of androgen production by retinoids may contribute to ovarian hyperandrogenism in PCOS. In general, the pathways involved in cell-specific retinol and retinoid metabolism are not well known, particularly within the ovary. Further studies are necessary to determine the pattern of expression of enzymes involved in retinol metabolism/retinoid synthesis in ovarian cells and their functional significance in retinoid action in PCOS.”
Potential role of retinoids in ovarian physiology and pathogenesis of polycystic ovary syndrome
https://www.sciencedirect.com/science/article/pii/S000989811730102X?via%3Dihub
“[...]abnormal retinoid signaling may be involved in the pathogenesis of polycystic ovary syndrome (PCOS), one of the most common ovarian endocrinopathies in reproductive-aged women worldwide”
So far, these are the questions I have (sorry in advance if Grant already answered any of these in his books, my memory is terrible at the moment):
- What qualifies as a “vitamin A deficiency?” (If you are “deficient,” RBP4 is not produced, which means vitamin A isn’t delivered to the peripheral tissues, including the epidermis.)
- Why does transthyretin bind both thyroxine and retinol?
- A gene called Stra8 (which stands for “Stimulated by Retinoic Acid Gene 8”) is essential for meiotic initiation during oogenesis—does this mean we actually do need at least some level of RA in the body or is there an alternative explanation?
- Could the PCOS theca cells have been initially damaged somehow by retinol?
- Is there any possibility that PCOS could be protective adaptation or some sort? (It does prevent pregnancy, which would be a good thing in the presence of vitamin A toxicity... I’ve also wondered if obesity is protective in some way as well, but I digress.)
- Any ideas about how genetics factor into this?
Okay, so I clearly don’t have much knowledge of human biology, and learned some new words today. 😝 But I thought the studies looked interesting, and I’m curious about them.
I have heard of people who have developed PCO/S after quitting oral contraceptives, like the pill. From what I understand, synthetic estrogens raise plasma retinol and retinol is also involved in aromatization of estrogen. This part I have not come to understand fully yet because the study's I have read have been very confusing. It seems retinol can inhibit aromatization which means less estrogen is being converted but at the same time it also seems that less estrogen is being converted from estriol to estradiol as well... Memory fails me, as I do not have the aromatization pathways in front of me or the studies. But just as you are trying to figure out pcos, i am trying to figure out endometriosis. Both are hormonal "dysfunctions" but very very different.
Grant has written a book about the link to breat cancer. I will devour that again further on to look at the studies. I believe there is a cause to every illness and I am determined to find and understand that cause. Breast cancer is, greatly, hormone related so there must be a connection to other hormonal issues as well. and when adding glyfosate, dioxins and xenoestrogens to the equation, it sure gets messy. Then sprinkle it with a bit of genetic differences in metabolizing estrogens (and others, like stress hormones) and we have ourselves a very complicated cocktail!
Puddleduck do you have pcos? And have you taken oral contraceptives in the past?
Quote from puddleduck on February 2, 2019, 9:56 pmFrom what I understand, there’s some connection between Polycystic Ovarian Syndrome and elevated Retinol Binding Protein 4 (the form of RBP in the plasma) levels.
I haven’t read the studies (it’ll take me days to do so for various reasons—I’m also not the best person to interoperate these anyway, since I’m not a scientist and I have to look up a lot of words along the way
), but thought I would post links to some of them (titles in bold above links, quotes below in italics):
Association between retinol-binding protein 4 and polycystic ovary syndrome: A meta-analysis
https://www.jstage.jst.go.jp/article/endocrj/61/10/61_EJ14-0186/_article
“Our meta-analysis results indicated that RBP4 might be a useful tool for identifying PCOS women.“
Retinoids and retinol differentially regulate steroid biosynthesis in ovarian theca cells isolated from normal cycling women and women with polycystic ovary syndrome.
https://academic.oup.com/jcem/article/90/8/4858/2838533
“The differential response of CYP17, CYP11A1, and STAR gene expression to retinoids in normal and PCOS theca cells further suggest that PCOS cells may have intrinsic differences in their ability to respond to retinoids as well as synthesize retinoids. Therefore, it is possible that stimulation of androgen production by retinoids may contribute to ovarian hyperandrogenism in PCOS. In general, the pathways involved in cell-specific retinol and retinoid metabolism are not well known, particularly within the ovary. Further studies are necessary to determine the pattern of expression of enzymes involved in retinol metabolism/retinoid synthesis in ovarian cells and their functional significance in retinoid action in PCOS.”
Potential role of retinoids in ovarian physiology and pathogenesis of polycystic ovary syndrome
https://www.sciencedirect.com/science/article/pii/S000989811730102X?via%3Dihub
“[...]abnormal retinoid signaling may be involved in the pathogenesis of polycystic ovary syndrome (PCOS), one of the most common ovarian endocrinopathies in reproductive-aged women worldwide”
So far, these are the questions I have (sorry in advance if Grant already answered any of these in his books, my memory is terrible at the moment):
- What qualifies as a “vitamin A deficiency?” (If you are “deficient,” RBP4 is not produced, which means vitamin A isn’t delivered to the peripheral tissues, including the epidermis.)
- Why does transthyretin bind both thyroxine and retinol?
- A gene called Stra8 (which stands for “Stimulated by Retinoic Acid Gene 8”) is essential for meiotic initiation during oogenesis—does this mean we actually do need at least some level of RA in the body or is there an alternative explanation?
- Could the PCOS theca cells have been initially damaged somehow by retinol?
- Is there any possibility that PCOS could be protective adaptation or some sort? (It does prevent pregnancy, which would be a good thing in the presence of vitamin A toxicity... I’ve also wondered if obesity is protective in some way as well, but I digress.)
- Any ideas about how genetics factor into this?
Okay, so I clearly don’t have much knowledge of human biology, and learned some new words today.
But I thought the studies looked interesting, and I’m curious about them.
Stephanie Seneff has an idea regarding PCOS @49:15