Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature may not be available in some browsers.
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
it did the opposite for me. I feel more emotional, my mood gets better and I have more libido after eating white button mushrooms. Probably I do react to something different. I have yet to test it but a few days ago when I (randomly) ate some pearled barley, I got instant cognitive improvement. The time period inbetween for is very similar with mushrooms. Then I learned both are rich in beta glucans. B glucans lower LDL. And since my steroid pathway is shitted beyond understanding this is very normal.There was a time for like a week I ate quite a bit. Killed all emotions in me, completely flat mood as well as killed the mental aspects of libido. This coincides with the fact that it is probably strongly anti-estrogen, despite possibly contradicting properties. Others reported similar.
Crashed Estrogen With White Button Mushrooms?
Hey everyone, Lately I have included a pretty large amount of well-cooked white button mushrooms in my diet because they are delicious and nutritious. I ate between 500-800g per day roughly. (raw weight) I noticed some things that I associate with low estrogen. I feel absolutely asexual and...raypeatforum.com
Agonism of 5-HT2C decreases dopamine and noradrenaline release in some areas of the brain. But fluoxetine is an antagonist of 5-HT2C unlike other SSRIs. Apparently 5-HT2C can also act without serotonin binding to it. This is known as constitutive activity.it did the opposite for me. I feel more emotional, my mood gets better and I have more libido after eating white button mushrooms. Probably I do react to something different. I have yet to test it but a few days ago when I (randomly) ate some pearled barley, I got instant cognitive improvement. The time period inbetween for is very similar with mushrooms. Then I learned both are rich in beta glucans. B glucans lower LDL. And since my steroid pathway is shitted beyond understanding this is very normal.
Mushrooms do something really good for my brain -- why?
White mushrooms pretty consistently are making my thinking "fuller" and more expanded. I doubt it's due to endotoxin reduction because oyster mushrooms and antibiotics don't have the same effect. Has anyone else experienced this and have any hypotheses as to why? The only thing special I could...raypeatforum.com
Mushrooms also contain copper and B5 (melatonin) and both can decrese serotonin. Copper is especially important here because I react badly to sugar (acidosis feeling) and I think it's due to that it's made of half fructose.
I'm trying to connect up cholesterol and HT2C (or serotonin). Are there any obvious interaction between this pathway and serotonin or GABA or noradrenaline?
These two papers (1 2) explains it all but I couldn't really grasp all of it. Fluoxetine is antagonist but it increases editing of 2C, decreasing its constitutive activity. It desensitizes them basically. The more edited types have low constitutive activity, have low G coupling and are located on cell surface while less edited ones have high constitutive activity, high G coupling and are located inside of the cell. 2C excitates GABA interneurons and GABA is a feedback to 5HT in that case and it's differently edited in amygdala. INI and VGV phenotypes are both anxious but what we know for certain is that fluoxetine increases editing though it also increases protein density of 2C so it's not just about mRNA editing. So as you see there are tons of things to consider.Agonism of 5-HT2C decreases dopamine and noradrenaline release in some areas of the brain. But fluoxetine is an antagonist of 5-HT2C unlike other SSRIs. Apparently 5-HT2C can also act without serotonin binding to it. This is known as constitutive activity.
Obvioulsy , instead of being on these serotonin lowering tdiets, you need to take care of your MAOs and all these problems will go away. No serotonin lowering regimen will cure any of you , since MAO is dependent on copper iron b2 and so on , and if you have lets say estrogen mimics inside your body as cadmium or mercury , your copper levels will be low so will be MAO-A and serotonin will be high . But feeding copper wont solve it, until your chelate mercury, since your body thinks you are high copper , when you are mercury toxic. All these diets are just cover ups of real problems and nothing more. You take care of your maos and everything will be nice and dandy again. Chelate chelate and chelate. Drink pure fulvic acid , chelate mercury cadmium and copper .
And progesterone wont help in these cases , yes it will level out metabolism but it wil make you even more copper deficient and zinc toxic. Remember estrogen mimics are not copper based, but should be copper based, so your progesterone will be balancing fake estrogens and lowering copper even more
Progesterone retains potassium. Gbolduev has said this many times and its correct. Potassium loading raises aldosterone, ACTH, cortisol and would be expected to reduce progesterone since its not needed to retain potassium as much. High sodium intake reduces aldosterone, promotes sodium loss to balance potassium levels. Probably leads to higher progesterone levels as well.These two papers (1 2) explains it all but I couldn't really grasp all of it. Fluoxetine is antagonist but it increases editing of 2C, decreasing its constitutive activity. It desensitizes them basically. The more edited types have low constitutive activity, have low G coupling and are located on cell surface while less edited ones have high constitutive activity, high G coupling and are located inside of the cell. 2C excitates GABA interneurons and GABA is a feedback to 5HT in that case and it's differently edited in amygdala. INI and VGV phenotypes are both anxious but what we know for certain is that fluoxetine increases editing though it also increases protein density of 2C so it's not just about mRNA editing. So as you see there are tons of things to consider.
That one paper says corticosteroids increase turnover of 5HT and one of the 5HT2Cs role is inhibiting this. My understanding is that if 2C is high this could cause feedback inhibiton of ACTH (my acth was lowish). I feel acutely bad on 5HTP and get better later. Some other study also states estrogen and stress have same hypophagic effect and 2C antagonism can reverse both. There is also this page saying 2C agonism can decrease some estrogen def symptoms. The thing with estrogen is that it's made with copper inside body and sense of excess estrogen causes body to waste copper and cause copper deficiency.
Here he says progesterone balances estrogen by retaining zinc and wasting copper. Part of my blood results look like this:
Progesterone - 0,52 - 17/01/19
Estradiol - 42 - 17/01/19
Progesterone - 0.98 - 09/02/21
Estradiol - 27 - 09/02/21
Copper - 90 - 09/02/21
Zinc - 104 - 09/02/21
Copper and Zinc are not out of the range but progesterone even on 0.52 is 2x folds high for some reference ranges I found on the internet. And It doubled in 2 years. E2 is not very consistent, it actually seems high but lowered later but anyway. I suspect these are all the downstream effect of fluoxetine's altering on 5HT2C receptors.
I bought KCl long time ago. Actually I first tried Light Salt which has 50%50 Sodium and Potassium. I noticed increased stress. Couldn't continue doing that because it made my bowel sound/contraction/jerking issue go haywire the instant it goes into my bloodstream (By the way since I have stopped dairy that problem almost vanished or become bearable). Not KCl but potassium in any food like bananas and potatoes too so I tried to avoid them. Sodium lessened that so I still suspect this is kind of renin-angiotensin-aldosterone problem that's breaking my sympathetic/parasympathetic balance. I sweat excessively, my pupils are dilated, my heartbeats used to be much more quiet so I think in general it shows me as sympathetic dominant.Progesterone retains potassium. Gbolduev has said this many times and its correct. Potassium loading raises aldosterone, ACTH, cortisol and would be expected to reduce progesterone since its not needed to retain potassium as much. High sodium intake reduces aldosterone, promotes sodium loss to balance potassium levels. Probably leads to higher progesterone levels as well.
If you wanted to normalize progesterone, potassium is the answer.