My practice consists of all type 2′s (it just fell out that way because of the population that I care for by age). Although I have learned about these new drugs I have not rushed to use them. I have worked in this office for 4 years. When I started there fewer than 1/4 of my patients with diabetes had a HgbA1C less than 8%. Today 1/2 are under 6.5% and another 1/4 of them are between 6.5 and 8%. The vast majority of them are on a combination of an old sulfonyurea, Amaryl, and metformin. Those who need it also use the long-acting insulin glargine (Lantus). I like Amaryl because it matches pancreatic insulin stimulation/secretion to meal time glucose excursions, rather than pushing the pancreas to make more insulin all the time. I believe that this helps to spare the pancreas from constant stimulation, possibly extending it’s usable life. Metformin, of course, helps the body to use insulin more efficiently. Insulin is what the body makes naturally to control blood sugar, so one can hardly argue with it’s use. My point is that there are drugs available already that can give great blood sugar control, and we should not rush to try new meds when they come out, just because they are avaliable. Studies of medications are very controlled in their choice of participants in order to minimize the risk of side effects. This ensures that there will be many new side effects seen in the post-marketing tracking once a new drug is launched. Each person has to choose for themselves whether or not a new drug is right for them. If one can achieve good control with their current medications and an honest effort at good eating an exercise habits, they may choose not to try a new medication the minute it hits the market. Once a full safety profile has been documented and you need a new drug in yor arsenal, you’ll still be able to choose that medication, unless it has been ripped from the market by post-marketing outcomes. Then you’ll be glad you avoided it!

Laurie

Anecdotal reports accompanied by plausible physiological mechanisms scare me a lot more. Which is why the info in Jenny’s Januvia pages
http://www.phlaunt.com/diabetes/18538604.php
really concern me. Messing around with the incretins sounds like a good idea. Messing around with DPP-4 sounds not so good. DPP-4 is a protein with two faces. On one hand, it’s an enzyme that slices up proteins, disabling them. Januvia works by disabling DPP-4. That way, the incretins don’t get sliced up and they stay around longer. That’s good. But DPP-4 apparently disables a lot of other proteins, which are ill-characterized. That sounds less good; we don’t know what we’re monkeying with.

Also, DPP-4 has another completely different role, sitting in the cell membrane and acting as a signaling site in the immune system. We really don’t understand what it’s doing there. Disabling it seems very much like “Hey, what happens if I push this button?”