Changexpert
Senior Member
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I have been trying to figure out different hormones effects on our bodies in the past few days. After some research combined with my past experience, I do not think DHT is the main problem for me. Whenever I used DHT inhibitor (saw palmetto, beta-sitosterol, and even finasteride), my hair would shed massively along with decreased libido. My serum DHT level has never been elevated, and it was always in the middle range. Scalp DHT level might be different, and maybe I am just susceptible to androgen activities once DHT binds to its receptor. I am not denying that DHT is a problem. What I am saying is that DHT is only one piece of the puzzle, and it does not seem to be the biggest cause for me personally.
DHT has been scapegoat for both hair loss and prostate cancer, but long-term efficacy cannot be guaranteed along with severe side effects. Also, 5-a reductase is not the only means of T converting into DHT, and there's a high chance that our body can adapt to produce DHT via different pathways, even if 5-a reductase enzyme is blocked. (http://www.nature.co...s/srep01528#f1)
I think just looking at DHT is a very narrow-minded approach for both hair loss and prostate cancer perspective, ignoring the benefits of DHT. I've seen a comment/blog post that DHT helps metabolize estrogen, but I have not done much research on this yet. Something else beyond DHT has pro-inflammatory effect in the body, and the best example of this would be castration resistant prostate cancer (CRPC), Even after castration, prostate cancer keeps growing, in the absence of androgen production.
Taking a different perspective, some researchers have shown that too much estrogen activity can be a problem for both hair loss and prostate cancer. Looking at my genes, I think this approach makes much more sense than DHT approach. A lot of my liver enzymes are defective, especially CYP1B1 genes. My total estrogen level was elevated at 139 pg/mL when I was not using an aromatase inhibitor. My estradiol level is on the 70th percentile as well. On the other hand, my progesterone is always low. COMT is also involved in estrogen metabolism, which I am defective in as well. Also, SAM-e is heavily involved in excreting estrogen out successfully, but I have a genetic defect in MAT1A gene, slowing down the conversion of methionine into SAM-e. This means my SAM-e level is naturally low, which worsens estrogen metabolism problem.
In addition, I've read a blog post about xenoestrogen, how fake estrogens in the body can mimic estrogen activities while not showing up on the blood test due to different chemical composition. If estrogen is indeed a problem, this would explain my timid personality as well. One question I have is do progesterone, estrogen, and DHT compete for receptor activities? I have read several comments and blog posts about progesterone competing against estrogen and estrogen competing against DHT, but I am not sure how this works. AFAIK, all three hormones have distinctive receptors (PR, ER, AR), so I am not sure how they can possibly compete for each other.
Estrogen overload is also seen regularly in women with breast cancer, so as always, balance is important. It seems like certain supplements that increase phase I pathway of liver would be helpful to convert estrone into less harmful compound. Anything that helps with COMT (SAM-e, magnesium) would increase the estrogen excretion.
Genes that are affected for estrogen metabolism
If you have any experience or thoughts on this topic, please share them! Thank you.
Post on xenoestrogen - fake estrogen
http://www.gestaltre...ealth-epidemic/
Estrogen metabolism pathway
http://www.marketfunctionalmedicine.com/wp-content/uploads/Estrogen-and-nutrition.png
DHT has been scapegoat for both hair loss and prostate cancer, but long-term efficacy cannot be guaranteed along with severe side effects. Also, 5-a reductase is not the only means of T converting into DHT, and there's a high chance that our body can adapt to produce DHT via different pathways, even if 5-a reductase enzyme is blocked. (http://www.nature.co...s/srep01528#f1)
I think just looking at DHT is a very narrow-minded approach for both hair loss and prostate cancer perspective, ignoring the benefits of DHT. I've seen a comment/blog post that DHT helps metabolize estrogen, but I have not done much research on this yet. Something else beyond DHT has pro-inflammatory effect in the body, and the best example of this would be castration resistant prostate cancer (CRPC), Even after castration, prostate cancer keeps growing, in the absence of androgen production.
Taking a different perspective, some researchers have shown that too much estrogen activity can be a problem for both hair loss and prostate cancer. Looking at my genes, I think this approach makes much more sense than DHT approach. A lot of my liver enzymes are defective, especially CYP1B1 genes. My total estrogen level was elevated at 139 pg/mL when I was not using an aromatase inhibitor. My estradiol level is on the 70th percentile as well. On the other hand, my progesterone is always low. COMT is also involved in estrogen metabolism, which I am defective in as well. Also, SAM-e is heavily involved in excreting estrogen out successfully, but I have a genetic defect in MAT1A gene, slowing down the conversion of methionine into SAM-e. This means my SAM-e level is naturally low, which worsens estrogen metabolism problem.
In addition, I've read a blog post about xenoestrogen, how fake estrogens in the body can mimic estrogen activities while not showing up on the blood test due to different chemical composition. If estrogen is indeed a problem, this would explain my timid personality as well. One question I have is do progesterone, estrogen, and DHT compete for receptor activities? I have read several comments and blog posts about progesterone competing against estrogen and estrogen competing against DHT, but I am not sure how this works. AFAIK, all three hormones have distinctive receptors (PR, ER, AR), so I am not sure how they can possibly compete for each other.
Estrogen overload is also seen regularly in women with breast cancer, so as always, balance is important. It seems like certain supplements that increase phase I pathway of liver would be helpful to convert estrone into less harmful compound. Anything that helps with COMT (SAM-e, magnesium) would increase the estrogen excretion.
Genes that are affected for estrogen metabolism
- CYP1A1 - downregulation, produces less of good metabolite 2-OH E1 (E2)
- CYP1A2 - downregulation, same as above
- CYP1B1 - downregulation of xenoestrogen metabolism, produces more harmful metabolite 4-OH E1 (E2)
- CYP3A4 - downregulation of breaking down various hormones, produces more harfmul metabolite 16a-OH E1
If you have any experience or thoughts on this topic, please share them! Thank you.
Post on xenoestrogen - fake estrogen
http://www.gestaltre...ealth-epidemic/
Estrogen metabolism pathway
http://www.marketfunctionalmedicine.com/wp-content/uploads/Estrogen-and-nutrition.png
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