Post #299 - Now if THIS Ain't a Load of Shit

I'm a caffeine drinker. I can't stand coffee, but I've been known to polish off between one and two 2-liter bottles of Mountain Dew a day. A DAY, PEOPLE. That's a lot of fucking caffeine. I should piss, shit, and BLEED neon yellow, I drink so much of it. I buy it 4 crates at a time (you know the blue crates Pepsi ships bottles in, 8 per crate???). I have to write Dew purchases into my monthly budget, to make sure I have enough to supply my habit. I don't bother with a glass, drinking directly from the mouth of that 2-liter bottle. I am a Dew addict. I need my fix. I didn't even curb my habit while pregnant with each and every one of my kids, and they should also shit, piss, and BLEED neon yellow after 9 months of continuous Dew infusion via umbilical cord. My kids are all above average in intelligence, motivated, and of the type to take a leadership role rather than that of a sheeple. I owe it all to the Dew. Look at that: Even my fucking CAT is addicted to this stuff.

Then along comes this study, claiming "Caffeine could protect against multiple sclerosis," which I would have to say based on my own real-life personal experience spanning 35 years , is a load of shit. I AM caffeine, I have been for years, and I still developed MS and it's still progressing. Give me some GOOD news, and let me know when you've really got something worthwhile, eh?

Researchers at Cornell University showed that giving mice the equivalent of six to eight cups of coffee a day protected them against experimental autoimmune encephalomyelitis (EAE), the animal model of MS. . .
Initial studies led the researchers to discover that mice lacking CD73, the enzyme necessary for synthesizing extracellular adenosine, were protected from developing the mouse form of MS (experimental autoimmune encephalomyelitis or EAE). Subsequent studies dealing with immune cells from such mice made them believe that normal CD73's ability to synthesize extracellular adenosine governed the development and progression of the MS-like disease.
Though this discovery did help the researchers to explain the presence of adenosine near the cells, but they were unaware of the mechanism that made the compound enter into the CNS cells. As adenosine is supposed to bind to its receptor in order to affect a cell, the researchers thought that adenosine receptor activation would have allowed for entry of immune cells into the brain and spinal cord and thus they turned to caffeine.
Caffeine's stimulatory effects on the CNS are mainly due to its ability to bind to the same receptors as adenosine, thus blocking adenosine's ability to affect CNS cells. When mice consumed caffeine in their drinking water, they were protected against development of EAE, the MS model.
Thus it was concluded that CD73 and adenosine receptor signalling are required for the efficient entry of immune cells into the CNS during the initiation and progression of EAE in mice and, quite possibly, during the development of MS in humans.