Tianeptine | This French Antidepressant Wonder Drug Reverses MDMA Induced Brain Damage [SSRE] скачать в хорошем качестве

Tianeptine | This French Antidepressant Wonder Drug Reverses MDMA Induced Brain Damage [SSRE]

Tianeptine In this video I’m going to be discussing what I deem to be the most powerful compound I’ve ever discovered for combating depression. That compounds name is Tianeptine First though, I have to mention that I am not a doctor, and anything I discuss in this video is for research and entertainment purposes only. The compound discussed in this video should not be consumed by anyone who resides in a country where this compound is not for human consumption. The legality of this drug differs depending on what part of the world you live in, so always check with the laws of your country before consuming anything. So let’s dive on in. Tianeptine is an antidepressant that was first formulated in France. It was patented under the brand name “Stablon” and “Coaxil” It’s an atypical antidepressant which is used mainly in the treatment of major depressive disorder, although it may also be used to treat anxiety, asthma, and irritable bowel syndrome. So there are multiple mechanisms of action going on with Tianeptine that can be a little confusing, but by the end of this video it should make sense the purpose each action serves working synergistic-ally to have the profound affect that it has. Tianeptine is a Serotonin Receptor Antagonist It’s a serotonin re-uptake enhancer and it also has an affect on the mu-opiate receptors Normally when you think of an antidepressant drug, you assume it’s something you take when the depression gets really bad, or more commonly something like an SSRI that you continue use for the rest of your life. But this was the first thing I discovered where people were talking as if it resolved there depression to the point where they no longer needed the drug. So naturally I had to try it. In modern medicine, our current model of depression is that it’s caused by a lack of serotonin. So we treat it with SSRI’s like prozac or paxil. For those who don’t know, an SSRI is a Selective Serotonin Re-uptake Inhibitor. To understand this we first need to delve into how serotonin works. Serotonin is labeled the “feel good” neurotransmitter. It’s released as a reward signal after accomplishing something allowing you to relax and feel good. Of course there are hundreds of other functions it’s associated with in the body, but we’re just going to focus on the pleasure aspect of it since depression is basically identified as a lack of pleasure or joy. So, you accomplished something great, your brain (and gut) releases serotonin into the synaptic cleft which is the space between the serotonin supply chamber and the serotonin receptors. Some of that serotonin flows to the serotonin receptors, however, your brain has natural regulation system, so some of the serotonin is picked up by what is called the re-uptake transporters. The brain has a natural regulating mechanism to make sure you’re not using too much serotonin at once and being wasteful with it. So this keeps your reserves from running out by you using it all at once, and also keeps you from over-saturating the receptor sites. What an SSRI does is it comes in and blocks the re-uptake door so the re-uptake transporters can no longer do their job of regulating the serotonin amounts being used at once. The result is you end up with more serotonin in the cleft to saturate the receptors resulting in depression relief from that large surge of serotonin. The problem is, and this is what you’ll discover if you ever take and SSRI or have ever spoken to someone who is on one, is the depression relief is temporary, and they then have to continue increasing the dose more and more, and often end up at a point where it stops working altogether regardless of dosage. Now that you see how an SSRI is working, it doesn’t take a rocket scientist to see why that occurs. Of course you’re going to eventually run out of serotonin in the reserves. But something else occurring as well which flips our whole depression model on its head once discovered. And that’s something called serotonin resistance. When you over-saturate the receptor sites with serotonin, the receptor site down-regulates and becomes resistant, meaning you now need more serotonin to get the job done. And this is obvious when you contrast it with other disorders in the body such as diabetes. They're seeing it as a lack of serotonin problem, but they’re completely overlooking the serotonin resistance which is the cause of the large demand of serotonin in the first place. If you could lower the serotonin resistance, you wouldn’t need to increase serotonin levels by blocking the re-uptake. Instead of focusing on increasing serotonin levels, how can we increase our sensitivity to it? Thanks for watching!