These are questions for anyone who would like to debate me as to the safety of Venlafaxine. I will debate anyone at all on any forum. Just like Hillary Clinton, I’ll even give you the questions ahead of time. It won’t matter, you’ll still lose the debate. Anyone, Harvard, PhD’s, anyone, I’ve defeated them all privately.
Question 1:
Venlafaxine and Tramadol differ by one carbon atom only. Morphine and Codeine differ by one atom also. We know that the added carbon in Codeine is demethylated in the liver which makes Codeine the milder opioid. What is the exact biochemical reason that Venlafaxine is neither a mu1 binding opioid nor an NMDA antagonist whereas Tramadol is both?
(a) the added carbon of Venlafaxine masks the activity of the phenyl group and hence it doesn’t bind
(b) the added carbon of Venlafaxine changes the polarity of the molecule such that it no longer binds
(c) the added carbon of Venlafaxine causes Venlafaxine to mirror a known antigen and is removed by the immune system when close to opioid receptors
(d) the added carbon of Venlafaxine causes a ‘folded chair’ configuration of the cyclohexane ring and blocks binding.
(e) there is no significant difference between Venlafaxine and Tramadol. Both bind similarly. This wasn’t detected due to dogmatic thinking, silo’ed development of both drugs, silo’ed approval and inadequate safety measures
Question 2:
PCP (Phencyclidine)
Question 3:
Question 4:
Question 5:
Question 6:
Ciramadol:
Question 7:
Source: Volpe-Ranking-of-opioid-affinities-for-Mu-receptor
The opioid binding affinity (Mu1 Ki) is known to be 10,000 for Venlafaxine which was noted as ‘negligible’ in it’s original study which was later altered in the drug safety sheet and citing literature to be ‘absent’ affinity for the opioid receptors. Which other known opioids bind with that same affinity? Were those opioids considered opioids when Venlafaxine was approved? Which of those opioids are scheduled? When were they scheduled? Were they all considered mild and not habit forming originally?
Regarding your statement in questions 7, “The opioid binding affinity (Mu1 Ki) is known to be 10,000 for Venlafaxine which was noted as ‘negligible’ in it’s original study”. Where have you found this data? The earliest published study I found from 1986 doesn’t support your statement – https://www.ncbi.nlm.nih.gov/pubmed/2998818
Yours sincerely, C
I can’t get access to the original paper at the moment (citation provided below). In the original paper, it cited opioid binding affinity as > 10,000 nm. Can you access any first hand sources that cites the exact binding affinity for Venlafaxine? I’d appreciate any first hand sources you can provide. I’m trying to catalogue them. The study you sent wasn’t a displacement test for drug safety, it was a test for effects in a particular tissue (area of the brain).
Here is the original paper used for drug safety. This is where I read it. I can no longer access the full text of it. If you can, kindly forward me a copy.
https://www.ncbi.nlm.nih.gov/pubmed/3790168
EFFEXOR is evil. It is like the evil witch in the movie with the grimm brothers where she plunges a sword in the heart of people and revives them but then when she pulls the sword back the person dies. EFFEXOR is the same, it removes suicidal thoughts from your mind but you have to pay a high price, you have to give away your IDENTITY.
You know who I am. Please open the mail to explain to you why ECT is not lowering the suicide rate. You don’t know the whole story/picture.