Awor told us a long time ago that the receptors themselves were working and binding the problem is signaling downstream, the end product and that is gene “expression” and it is not there…
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What about the qeeg tests and fmri tests. I think I’ve seen 4 ppl take them across all forums and 3 said brain damage consistent with a tbi. 1 said no damage. Still wouldn’t explain windows (I haven’t had any), and bettering / worsening of symptoms
First question: My understanding is that the overexpressed AR create misshaped proteins. I’m guessing that’s what’s causing the lack of expression.
Your second question: The second part of the study was far more evasive, painful, and had stricter criteria. So I’m guessing some patients opted out or didn’t meet the criteria.
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could you post here the simple explanation for me that I am ignorant about these things so scientific?
thank you.
and I have another question, is it possible to answer badly to testosterone (I have high base testosterone) but to answer well to hcg 250 ui?
thank you
I don’t think hes paid hes just an idiot.
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I’m sorry I am not a scientist and I don’t quite understand your question(s). I only have a layman’s interpretation of things.
There are some fantastic YouTube videos that illustrate what transcription and translation is, and the end result – the protein – and how it can be misshaped. I recommend watching those for a better understanding.
I feel that the best hope for an intermediate form of treatment which can be a stopgap before any feasible epigenetic cure would be addressing the deficiency of neurosteroids. The admin team making decisions about future research initiatives have to weigh up where to best direct resources. Assuming resources are finite (which they of course are) there are two alternate paths as far as I can tell.
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Direct efforts into better understanding the unique genetic signatures which predispose people to get PFS. Then the next step would involve attempts to create an animal model which could then, in the future be used to trial a wide variety of treatments, many of which would be too risky to try on human sufferers. Any epigenetic treatments would first need to be trialled on animals as it’s far too risky to do so on humans.
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Direct efforts into addressing known deficiencies that PFS sufferers have in preference to understanding the aetiology of the condition. Things such as trialling allo analogies on human subjects, which is a relatively low risk undertaking.
I’m not pretending that it’s an easy choice. However I am personally of the opinion that focussing on something which could potentially being relief in the next few years would be a wiser approach than something which has a 10 year timeframe. 10 years is a hell of a long time to suffer.
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Yes, missed opportunities, you’ve all probably had some already.
whether its a girl, job, or moment in time where you didn’t do the right thing or make the right choice.
Some opportunities or chances might come around only once in a lifetime.
Did you make the most of this time?
Obviously the time is now for everyone, even with any type of so called cure, you dont want to wake up one day and be like “Man this is great, Im ready to live my life again!”
“Oh shit, im 50.”
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Lots of gurus who used to be around here we haven’t heard from…
Is this a toxic gain of function??
Is this a toxic gain of function??
What does this mean?
So now that we have scientific grounding, I feel as though this article is more relevant than ever
https://www.nature.com/articles/s41388-020-01598-0
Thoughts?
I don’t think people here are qualified to discuss this.
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44 clicks and no comments.
What are your thoughts?
Loss and revival of androgen receptor signaling in advanced prostate cancer
^How do you relate this to the PFS study?
Hard to draw any conclusions at all. As far as we know we haven’t lost AR signaling (in penile skin atleast).
We didn’t undergo ADT, but rather ALT (androgen lowering therapy). We don’t know if the cells would adapt similarly to ADT if there’s still circulating androgens.
And the therapy they are discussing is only done in vitro so far.
Edit: If anyone with PFS donate some prostate tissue to get examined and they find out a decrease in AR it would become real interesting though.
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95% of this place’s discussion falls under that
if im not wrong, the same people who were correct about the baylor research before it dropped, also said that the connections to the AR signaling problem in prostate cancer would be similar to our situation.
they also consulted steroid biologists and other scientists. i get what youre saying, its all still uncertain, but suppose its similar, i think the article is interesting.
We’ve wasted nearly two decades with mental masturbation and other pseudointellectual ramblings. It’s time for Direct Action.
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How about this one?
AR overexpression could equal persistent AR signaling.
How about over persistent AR signaling?
That becomes pathological.
We’ve also wasted a lot of time in lecturing people without actually producing results ourselves
It’s time to go make things happen rather than telling others to do something from the comfort of your chair
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