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For months ive had some weird nipple pain. I think its gyno developing. I don't mind because with a little exercise ive gotten it under control.
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I bought SJW a few days ago (haven't taken any yet). It was at a herbal medicine store (you probably have those in your neighbourhood too) but the women who sold it to me seemed to know a little bit about SJW. She asked me what i was going to use it for (as you probably already know, it's mainly used for treating depressia/anxiety), if I knew what SJW actually did and if I knew that I couldn't use anti-depressions and some other medicins together with SJW. I said "yes I know, but I'm actually going to use it to get my liver to process faster so that certain things will be out of my system quicker."
She had no idea why I would do that, but telling her the whole story about RU etc was going to take a lot of time and effort which I didn't want to spend on it. So anyway, she gave me the SJW and I asked her wether I could use it for a life-long period of time. She said I certainly could not take it for the rest of my life, let alone a couple of years. However, up to 6 months would be fine. Maybe 1 year too, but that was pretty much the max according to her.
Now I'm doubting her knowledge a little bit, but I can definitely see why one shouldn't take SJW for the rest of their lifes. Besides, it works as an anti-depressant believe and taking those for a very long time can affect your body I believe. There is actually quite a lot of debate about this because the long term (side) effects of anti-depressants are unknown.
So using SJW for a long time is out of the question. Maybe you could do a couple of months on and a couple of months off? I guess this also depends on how effective SJW is in reducing sides and on how bad your gyno is going to be if you let it run loose a few months. Also, I don't think taking an overdose (like Boldy is doing) is a good idea. But that's just my gut feeling though.
About your second point, whether RU is still going to be as effective: I don't know. Theoretically, RU doesn't have to go systematic to be effective I believe. This would mean that if it would never even pass the liver, it would still be as effective. So therefore I don't think that using SJW is going to affect the efficacy of RU. This is just logical reasoning though (broscience for the win), I could be wrong.
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I was thinking as of late... Couldn't we use any DHT-supplements or anything? For example, some brands of creatine cause spikes in your DHT levels. Or anything along those lines? I know it seems kind of a dumb idea, inhibitting DHT on your scalp for hair loss and boosting your systematic DHT at the same time, but still... Might be worth a shot? I don't really know of any DHT-supplements though and I'm fearing those supplements are too weak to do anything... But maybe you can "restore" the balance in your body once again by using RU and DHT-supplements at the same time?Comment
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Another thought popped in...
RU is stopping a certain %age of T and DHT from binding to the hair follicle right?
So if RU will go systematic, does that mean that it will both reduce your T and DHT?Comment
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Jup. Thing is RU58841 half life is extremely short, 1 hour. When you apply it to your skin RU58841 is already being metabolized immediately to an inactive metabolite which has a way weaker affinity to the androgen receptor. Btw it will never touch your hormones, just targets the androgen receptor. It won't mess with your production of hormones.Comment
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Illusion, thanks for the response. it answers a lot of questions. I agree SJW seems to be to good to be true as a problem-free way to get rid of potential Anti-Androgen sides.
Also, your DHT theory sounds good on paper, but we have no idea if that will work. It definitely would be counter-productive for finasteride, though. However, I don't think it's a good idea to be messing with the hormone balance that much. One medicine is already risky enough, I wouldn't try to counter Ru sides by adding another factor which we have no idea about the side effects. However, if one was willing to try it I'd be interested in the results. But honestly, I'd be so hard the gauge what was going on. You'd have to be 100% certain about previous Ru sides, and again be 100% certain that it was the external DHT that took them away. There are cases when sides reside by themselves through time as the body adjusts.
I think the best route for A-A is just to be ready for the sides. If my gyno from topica fin gets better, I will try Ru again at a very very low dosage like 15 mg.Comment
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Well, there goes my theory about increasing DHT production. If you say it doesn't touch our hormone production, it doesn't matter how much we produce anyway. It also means that we shouldn't be looking into the "change your hormone level" route to combat RU sides, which by the way isn't a very desirable route to go down in the first place.
But what I don't get is the following: If the half life is that short and if it's being metabolized to an inactive metabolite immediately when going systematic, then why are some people experiencing side effects? Or let me put this more clear, why are some people experiencing side effects throughout the whole day and not just the first few hours (when most of the RU is still in our bodies)?Comment
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Yeah I am affraid you're right. It's a shame though, I saw RU as my last resort but now even my last resort seems kind of a bad option. I guess it's no different from you.
How bad is your gyno? Is it on both sides? I only have gyno in my right nipple, something that really baffles me tbh. My androgen receptors must be way more sensitive in my right nipple or something weird like thatComment
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A compound for instance can have a half life of 3 hours but only stay bound to a receptor for a few minutes. Read this article it will let you understand more of it; http://www.pharmaceutical-journal.co...065576.article.
Studying how long a drug stays bound to a receptor can help scientists develop more effective medicines.
One of the best-selling antihypertensive drugs candesartan lowers blood pressure more effectively than any other drug in its class. One possible reason for this effectiveness is its binding kinetics: the active agent spends several hours bound to its target receptor, the angiotensin II receptor, compared with just a few minutes for losartan — another drug in its class.
“It has been postulated that for this reason candesartan is advantageous because it produces more prolonged blood pressure lowering, meaning that it has greater efficacy at lower doses and retains efficacy in the event of a missed dose,” explains Mike Waring, principal scientist at AstraZeneca, which markets the drug as Atacand.
Over the past five years, scientists have increasingly been studying drugs’ binding kinetics, which determine how fast a drug and its receptor associate (K on ) and dissociate (K off ). There is mounting evidence to suggest that the ‘residence time’ — a term introduced by Robert Copeland and colleagues at GlaxoSmithKline in 2006 to describe the time a drug remains bound to its target — has a strong influence on a drug’s clinical success.
Only 10% of drug candidates that enter phase I trials end up being approved by the US Food and Drug Administration[1] . To try to reduce this attrition, pharmaceutical companies have started studying binding kinetics in drug discovery programmes, but this is not yet being systematically applied because of a lack of experience and uncertainty about its importance.
“Until recently, binding kinetics has been ignored — the least we can do is pay more attention to it,” says Ad IJzerman, a medicinal chemist at the University of Leiden in the Netherlands. “We want to convince the research community you can’t live without it.”
Molecular basis
The concept of binding kinetics dates back to work in the early 1960s by William Paton, one of the pioneers of pharmacology [2[9]] [3] . In one paper, Paton postulated a rate theory, which uses the interaction of a drug with its receptor to explain drug action, potency and speed of offset3 .
Several important advances have since led to the current interest. In 1984, Motulsky and Mahan laid the theoretical foundations for binding kinetics and outlined the equations used to measure it[4] . And in 2004, David Swinney highlighted the importance of the biochemical mechanism of drug action in drug efficacy and safety[5] .He described the potential discovery and development risks associated with the binding mechanism of drugs and proposed simple rules to minimise them.
However, researchers have tended to focus on the strength of the binding between a drug candidate and its target (the affinity), rather than on how long the drug remains bound to the target (the residence time). The affinity of a drug is the concentration at which 50% of the target receptors are occupied. This is the ratio of K off to K on but says nothing about the binding kinetics.
“Initially, researchers believed that if a drug has good affinity, it would have a good effect. But this is not the case,” says IJzerman. “You can have a good website, but if you don’t stick to its pages long enough, you probably won’t have learnt that much.”
He explains that two drugs can have the same affinity to a receptor but have different binding kinetics, and these may affect the drug’s efficacy. “If you focus on affinity alone, you’d have difficulty in selecting promising drug candidates,” he says.
Four key factors are thought to play a part in controlling drug–receptor binding kinetics at a molecular level: molecular size, hydrophobic effects, electrostatic interactions, and conformational fluctuations[6] .
“It has been observed that as you increase the hydrophobicity of a drug, it creates a higher energy barrier; in other words, it makes it harder for the drug to dissociate from its receptor,” says Waring. “The hydrophobic parts of a drug are shielding the hydrogen bond from the water.” He adds that the conformational flexibility of a drug is also being studied to see how it affects the binding kinetics. In general, more flexible compounds tend to have longer residence times at the target receptor.Comment
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Good question. Biology isn't math. Pharmacokinetics (http://en.wikipedia.org/wiki/Pharmacokinetics) studies the moment from when a drug is administered to the point it is eliminated from the body with rough models. Note how I say "rough". Thing is everybody is different. Such models give only an approximation. The real actual half life can differ between different people. Enzymes of a person for instances are involved often in metabolism of various drugs/compounds. The quantity of these enzymes varies according your genetics. So the fact that RU58841 calculated half life is 1 hour doesn't mean that it applies to your body, it may be longer, may be shorter. Same with other many drugs including finasteride.
Then we don't even get to the point of how people can react differently to drugs as you know. People vary greatly too in response to drugs in terms of side effects. We all just have different genetics.Comment
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My gyno is on both sides. However, it seems to be stronger on the left side. It seems like it will deflate for a few days here and there and then flare back up. I hope it goes away in a couple of months, this is really holding me back from going on Ru again.
Thanks for the answer, Swooping. I will be reading that.Comment
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Swooping, would you happen to know the life time of fin in the system? How long after one quits would it leave the system completely. I reckon it would take a week or half for Ru.Comment
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