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Parental Thc Exposure Leads To Altered Striatal Synaptic Plasticity In The Subsequent Generation.


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Look guys it could be true and it could be false. There are aspects that need to be covered like which parent, age etc. I do agree that if you are going to use assume and expect that the preponderance of evidence should be overwhelming before making such a statement. How about they examine the behavior of children born to parents who reg smoked. It prob would not be conclusive but wold point in a direction. 

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I somehow hit the back button and my first response got deleted before I could post it.

 

I believe that information bias is an issue here. I'm not sure if my post or the reactions to it are more indicative of the problem.

 

Again, if the behavioral aspects of the study are pushed aside we're still left with brains that were analyzed that show a decrease in CB1 as well as other expression levels of receptors. Unless you're willing to accept without any evidence that these authors are presenting fraudulent data that doesn't seem to be open for debate.

 

There was really only one sound argument that I recognize in this thread and it was from the first post. How much did they use? I'd go further with that to ask for how long, and at what age? I'm not sure of the answer. But given the track record it's more than valid. I can't imagine that it would be difficult to give a very young mouse (they say adolescent but I'm not sure exactly what that means) large and sustained doses of THC that retard its development permanently. 

 

As you may have noticed I linked a couple papers on epigenetics. That appears to be what's going on here. This seems like an important concept to try to understand and as those papers point out this understanding comes with great potential.

 

The ECS is directly involved in the pathogenesis of a number of diseases. Cannabinoids modulate gene expression. Epigenetics play a role in inheritable genes (and might be reversible). That means that cannabinoids might be useful tools in stemming diseases before they have a chance to develop.         

 

Is there a difference between the methods used in this study and the normal consumption of cannabis? How young does a human have to be and how much would they have to consume (and for how long) to permanently lower the expression levels of the receptors? What is the period of time it takes for an adult human that has been exposed to exogenous cannabinoids before their expression levels of receptors rise to normal levels? Is it possible to permanently lower the expression level as an adult? These are the questions that seem matter most to me.   

 

It seems worthwhile to move this discussion to the other thread, but you're your own landlord.

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I believed this before I ever read this study. I had a conversation about it with people from this board. Don't worry, they laughed at me too.

How was the THC administered to the rats? We have found that an earlier study (by this same group) administered THC intravenously, in a way that made the study invalid.
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