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First of all, it is important to distinguish the different types of proteases being inhibited. There are different classes
(serine-threonine, aspartate, etc.) In addition, to equate isoflavones derived from soy, for example, with the effects of a drug like bleomycin, say, (a chemotherapeutic), is a bit ridiculous. Unless one is taking a broader definition of chemotherapy. But then LSD or AZT or DHEA could all be "chemotherapy" since they are chemicals (in contrast to radiation or surgery).

The current drugs on the market referred to as protease inhibitors that are used to fight HIV have well characterized toxicities. They are distinct and dependent upon the protease. There is no question that these toxicities exist and that they add a significant caveat to their use.

Such apples and oranges comparisons really don't move things forward any in the slightest. The data from clinical studies, which one can accept or reject at will, clearly and consistently suggest people with under 50-100 T cells (thereabout in general) who go on combination therapy (indeed, call it chemotherapy, whoop-te-doo) see significant improvement and resolution of many clinical symptoms. I personally don't rely on data alone. I've seen it happen in many of my friends.

At the same time, I am VERY worried about the trend of treating people at higher T cell levels. Especially since I feel that there are many other options that are being ignored. This is cruel and stupid. And it's because of issues of profitability, not science.


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-Physician's Drug Handbook 7th ed reports that Ritonavir is 98 to 99% bound to plasma proteins. Indinavir is about 60% bound to plasma proteins. Saquinavir is about
98% bound to plasma proteins. If these drugs are binding to plasma proteins, then it is reasonable to assume they are binding to organ and tissue proteins as well. How else can one explain Crixivan kidney stones? Kidney failure? Nerve interference? Interference with clotting factor in hemophiliacs?

The protease inbitors are simply non-specific hydrophobic interface peptides that can bind anywhere to cause a constellation of side effects.

Since they seem to bind to serine proteases (not just aspartic proteases), there seems to be a clotting factor decrease in hemophiliacs. Rumors have it that hemophiliacs have to increase the amount of clotting factor used because of interference with the clotting cascade.

 


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