So in our previous caffeine articles, I went into detail on how caffeine works.
Today I will talk about how caffeine should not be taken with meth.
A (not so) Fun fact: An extremely popular drug combo of Meth and Caffeine, called Ya-Ba, is prominent in Southeast Asia. It, originally, was given to horses to provide them with a crippling addiction to meth, but also to help them when they were pulling carts uphill and other physically intensive work. For this reason, it was called Ya-maa, or horse medicine. However, when people took notice of how it increased the horses’ ability to party by 200%, they decided to hell with the horses! “If it’s good enough for a horse, well, it’s good enough for me!”
This beautiful looking horror pill has many names. The Madness drug, crazy medicine, crazy pill and horse party (No).
Yeah, so, don’t. Just… don’t.
Definitely a bad idea. Meth + Caffeine = bad things.
Actually, while I’m at it. You really shouldn’t take meth. That’s just…like…I mean it’s… it’s… Goddamn, it’s just a bad idea. Just, you know, avoid doing that altogether.
Interestingly, caffeine exacerbates the effects of meth, greatly increasing the potential for adverse side effects (Section 13.4). To put it simply, dosages of caffeine and meth that were considered non-toxic when taken separately, became incredibly toxic when taken together.
Meth in and of itself is pretty neurotoxic. Causing all kinds of exciting side effects. I’m not going to go into detail on how damaging this drug can be, so I will leave a little article here to view if you wanted to look at some more information regarding the long-term consequences of meth use.
Yet, another compelling reason as to why you shouldn’t touch it, lick it or bop it.
Anyway, speaking of hard drugs, there appears to be a surprising amount of positive research in support of caffeine and its anti-Parkinson effects. Which is in strong contrast to meth’s pro-Parkinson effects.
First, what is Parkinson’s? Parkinsons is a neurodegenerative disease that affects more than 60,000 people in the united states alone, and a total of 10 million people worldwide. Parkinsons is ubiquitous, unfortunately.
It’s caused by extremely low or no levels of dopamine. The Substantia Nigra of the midbrain is where the highest concentration of dopamine creating and releasing neurons are located. Dopamine is a neurotransmitter that is necessary for a multitude of processes within our bodies. Dopamine is primarily known as the “reward” neurotransmitter. Dopamine is released when you do things like, eat chocolate, have sex or do drugs. It’s also necessary for proper movement, regulation of mood and appetite, to proper sodium balance and gastrointestinal function to many other processes. Anything that causes damage to areas that produce or release dopamine can lead to higher chances of developing Parkinson’s later on in life.
The symptoms of Parkinson’s usually develop at a later stage in the disease, when a substantial amount of the neurons that are necessary for dopamine production and release have been destroyed.
Meth does that extremely well. If meth is good at anything, it’s destroying dopamine production. Pro-brain killer. A+.
Because of the damage that meth can have on certain areas of the brain, such as the substantia nigra, this can increase the chances of developing Parkinson’s later on in life because it induces cell death within the substantia nigra, which can lead to issues with dopamine production as well as the release of dopamine.
In contrast, the way that caffeine works in the brain, it can actually aid in preventing the development of Parkinson’s. It can aid in this because of how it works on those adenosine receptors we spoke about in part 2. It seems that because of how caffeine “blockades” the A2a receptor, which functions primarily in the area with the highest concentration of dopamine-producing/releasing neurons, it can aid in preventing damage to that area. This area is called the striatum.
Another interesting tidbit is that since they know what specific receptors caffeine acts on, they were able to figure out which receptor out of the two was responsible for the mild Parkinsons protection, by using compounds that were specific antagonists to those two receptors while also inducing damage to that area in mice. Those compounds that were antagonistic to the A2a receptor, were shown to be protective of that area, whereas the compounds that were antagonistic to the A1 receptor were shown to be ineffective and even worsened it.
I hope I explained that in an easy to understand way. If you have any questions, feel free to contact me!
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