Experiments
28/05/10 14:32
When we were first looking at BITC, we didn’t want to test it on CF patients, themselves. A lot of these kids, and adults, especially, are already sick, and the last thing that we wanted to do was make them sicker.
Don’t get me wrong—we were sure of our theories. I check, recheck, check again, recheck again, check another time, recheck my recheck. I’ve got whole entire abstracts memorized, I’ve checked so many times. I’m continually checking, because I am so scared of hurting someone. But, no matter how much checking you do, theories are often just the starting point, and you have to go back to the proverbial drawing board, over and over again, usually, no matter how good your theory is. It is, in fact, very unusual, to hit the jackpot and be right the first time around. That old adage, “A little knowledge is a dangerous thing,” rings very true, when it comes to theories.
Sooner or later, though, you come to a point where you have to test. No one in the mainstream scientific world was paying attention to our work. Oh, of course, there were some scientist writing to us their congratulations on our first paper. I guess they didn’t know who we were and that we had no credentials. But aside from that, no one was really interested. And, I think, too, that no one wants to test someone else’s work, because it costs money to test, and they couldn’t make money off of a patent that they didn’t have. So, we had to do the testing ourselves.
And we didn’t want to test on CF patients, so we tested on the next best thing: a carrier. But, what to test for? Carriers are not sick. Aside from the problems with the vas deferens, in some heterozygotes, carriers don’t have the pathology that’s seen in CF patients. And, of course, we don’t have the ability to test for potential difference, or chloride ion transport, or any of the other anions that are moved through the MRP or the CFTR. What to test?
We searched around the databases and saw that, sometimes, carriers had different fatty acid profiles than normal people. I don’t want to go too far into the reasons why, but it has to do with zinc transport to certain proteins that are responsible for the processing of fatty acids out of the membranes of the cells. Because the zinc homeostasis is screwed up in CF, the proteins that are responsible for the processing of arachidonic acid (AA) and docosahexaenoic acid (DHA) don’t work properly. Zinc is supposed to fit into one inhibitory spot on the protein that moves AA out of the membrane and it’s supposed to be picked up by the protein responsible for moving DHA out of the membrane. These proteins don’t work right because zinc homeostasis is messed up in CF. The end result is that you have too much AA, which is pro-inflammatory, and you don’t have enough DHA, which competes with AA for the cyclo-oxygenase cycle which, in turn, results in more pro-inflammatory compounds, prostaglandin E2 and leukotriennes. Long story, short, CF patients have more inflammation because of this. Now, don’t go and rush out and buy DHA. It helps, but because it is way down in the pathway for inflammation, and there are other factors that increase inflammation, it doesn’t work THAT well. And it doesn’t address the core problem. But, suffice it to say that, if you can effect a change in the fatty acid profile of a carrier, and especially in terms of these two fatty acids, you know that your compound is doing what it’s supposed to do.
So, we decided to test the fatty acid levels of our carrier. To start, he went in to his doctor and got some blood drawn, and sent it out to the lab, to get a fatty acid profile done on it. That gave us a baseline.
Then, he took BITC for one week. And he had his blood drawn again, and a fatty acid profile done on it. No change. So, he increased the dose – doubled it—for one week. Then, he had his blood drawn again, and the fatty acid profile completed on it. Voila!
Guess what happened? Can anybody out there guess? Which one went up, and which one went down?
Don’t get me wrong—we were sure of our theories. I check, recheck, check again, recheck again, check another time, recheck my recheck. I’ve got whole entire abstracts memorized, I’ve checked so many times. I’m continually checking, because I am so scared of hurting someone. But, no matter how much checking you do, theories are often just the starting point, and you have to go back to the proverbial drawing board, over and over again, usually, no matter how good your theory is. It is, in fact, very unusual, to hit the jackpot and be right the first time around. That old adage, “A little knowledge is a dangerous thing,” rings very true, when it comes to theories.
Sooner or later, though, you come to a point where you have to test. No one in the mainstream scientific world was paying attention to our work. Oh, of course, there were some scientist writing to us their congratulations on our first paper. I guess they didn’t know who we were and that we had no credentials. But aside from that, no one was really interested. And, I think, too, that no one wants to test someone else’s work, because it costs money to test, and they couldn’t make money off of a patent that they didn’t have. So, we had to do the testing ourselves.
And we didn’t want to test on CF patients, so we tested on the next best thing: a carrier. But, what to test for? Carriers are not sick. Aside from the problems with the vas deferens, in some heterozygotes, carriers don’t have the pathology that’s seen in CF patients. And, of course, we don’t have the ability to test for potential difference, or chloride ion transport, or any of the other anions that are moved through the MRP or the CFTR. What to test?
We searched around the databases and saw that, sometimes, carriers had different fatty acid profiles than normal people. I don’t want to go too far into the reasons why, but it has to do with zinc transport to certain proteins that are responsible for the processing of fatty acids out of the membranes of the cells. Because the zinc homeostasis is screwed up in CF, the proteins that are responsible for the processing of arachidonic acid (AA) and docosahexaenoic acid (DHA) don’t work properly. Zinc is supposed to fit into one inhibitory spot on the protein that moves AA out of the membrane and it’s supposed to be picked up by the protein responsible for moving DHA out of the membrane. These proteins don’t work right because zinc homeostasis is messed up in CF. The end result is that you have too much AA, which is pro-inflammatory, and you don’t have enough DHA, which competes with AA for the cyclo-oxygenase cycle which, in turn, results in more pro-inflammatory compounds, prostaglandin E2 and leukotriennes. Long story, short, CF patients have more inflammation because of this. Now, don’t go and rush out and buy DHA. It helps, but because it is way down in the pathway for inflammation, and there are other factors that increase inflammation, it doesn’t work THAT well. And it doesn’t address the core problem. But, suffice it to say that, if you can effect a change in the fatty acid profile of a carrier, and especially in terms of these two fatty acids, you know that your compound is doing what it’s supposed to do.
So, we decided to test the fatty acid levels of our carrier. To start, he went in to his doctor and got some blood drawn, and sent it out to the lab, to get a fatty acid profile done on it. That gave us a baseline.
Then, he took BITC for one week. And he had his blood drawn again, and a fatty acid profile done on it. No change. So, he increased the dose – doubled it—for one week. Then, he had his blood drawn again, and the fatty acid profile completed on it. Voila!
Guess what happened? Can anybody out there guess? Which one went up, and which one went down?