David and Micheal - thank you for the exchange of ideas. By trade I am an engineer and I see the body as a complex machine composed of interacting subsystems. Treating diabetes is actually a flow control problem. This is the approach "Engineer" Bernstein takes and also the approach Al Mann took when he developed the insulin pump. For "tools" Bernstein had a meter, glucose absorption rates of food and the speed of insulin, Mann had a computerized pump and sensors and again insulin speed. What both struggled with was the flow of glucose was out pacing the speed the insulins they were using to counter-act the BG spike. In other words they were limited by the insulin which was too damn slow.
With real time sensors and insulin which reacts like pancreatic secreted insulin addressing the flow control is not that complicate but needs to be tuned on an individual basis called titration. We have been taking a similar approach with IV insulin in hospitals for years monitoring real time through real time monitoring. You see it doesn't really matter what caused diabetes the end effect is damage to the pancreas has occurred and the body is not producing enough insulin for body signalling and glucose utilization.
The terms Type 1 and Type 2 are historical terms putting diabetics into two categories; those which needed to be put on insulin today or they will die; and those that can wait for some period of time before they need to be put on insulin. Prior to the 1960's T2's were seldom treated except with diet and exercise. Insulin was viewed as too dangerous and not worth the risk of hypoglycemia and killing the patient. The first widely used non-insulin sulfonylureas was Orinase introduced in the U.S. in the late 1950's. It really was not until Orinase and the potential for HUGE money by Big Pharma that a "T2" market was born.
I have so many studies on early insulin intervention they would fill a 4 draw file cabinet. Some of them date back to the 1950's and the last was about 6 months ago. They all basically say the same thing. There are huge benefits for the PWD with early insulin intervention. In other words skip the "Step" program and put them on insulin day one. However, there is much less money in this for Big Pharma. The T2 market is huge at least $30B and probably heading to $60B.
No Big Pharma wants this disrupted. In fact they will rush a product like trulicity to market hoping to grab the money from Januvia Byetta and Victoza if they lose their lawsuit and they get pulled from the market. That said truth is its all about the money with Big Pharma so PWD beware of the product you are taking. And, the fact is most doctors only know what the sales rep has told them. Diabetes treatment has changed so much in the last 5 years because of the real time sensors - CGM, cloud connection and a fast insulin which can mimic the pancreas. In fact,now I can sit in my office an watch real time a PWD arcoss the world and see their glucose profile thanks to Dexcom and the cloud. Thats only been available for a few years way after your doctor went to school.
As I mentioned, diabetes is a flow control problem. You will hear terms like "closed loop" when they are talking about the Artificial Pancreas. Now, the one thing all diabetics have in common is they are not producing enough insulin, regardless of the cause. The question is to what degree are they producing insulin to meet their glucose infusion needs? The answer to that is unique to the patient and can be measured with our real time sensors (CGMs) during a glucose test. The second question is are their beta cells still under attack from their immune system and if so how aggressively. The answer to that is answered with many different lab tests combined by ongoing monitoring. Again this will vary from patient to patient. Now we can call some people T1, and some T1.5 and some T2 and LADA and some MODY and some MODY-2 and even MODY-3 and a few more names. Whatever the cause and whether or not they have active immune system activity none of the PWDs are making enough insulin but some are making more than others.
We see people all the time get on this forum and say I was a T2 but now they say I am a T1. Or I was a T1 but then my BG was perfect and then a T1 again in the early stages of the immune system attack.
We can even debate whether "T2" is the result of insulin resistance as a result of diet and exercise and being obese. Now its my theory which I have no hard studies that almost all T2 is the result of some type of attack on the beta cells and the attack is mild enough that there is no trace in the immune system by the time testing is done for anti-bodies. Coupled with the insulin resistance the body can not recover without help. What we do know is T2s share genetic traits by gene type so we know there are more than a dozen different variations of T2 but again it does not matter unless we are doing research for a cure. I am not. I am addressing the flow control problem.
However, what I will say is we have a lot of obese people who do not have diabetes and when autopsies are performed on their pancreas they have grown big clumps of beta cells. We also have identical twins and they don't both always develop diabetes. So, clearly while genetics and insulin resistance play a role they are not the root cause of what attacked the pancreas and damaged the beta cells.
The problem in addressing the flow control problem is mimicking the pancreas but the insulin action with available "insulins" has always been TOO damn slow. Its all about how fast injected insulin will start to work and then how fast it will stop working. If you have a "tool" (insulin) which mimics natural pancreatic insulin action, you have the "Holy Grail" in diabetes treatment. You may not have cured it but now you can mimic natural insulin secretion and action.
Now Micheal said " BG readings have dropped dramatically and never goes over 125". If you are getting postprandial BG readings never going over 125 with Trulicity thats awesome. You are seeing non-diabetic numbers. However if that 125 is your fasting BG reading thats not great. What they did do in the studies is combined Trulicity with insulin - Lantus and usually quote those results saying significantly more people treated with Trulicity 1.5 mg plus insulin glargine achieved an A1C of less than 7 percent (69.3 percent) compared to placebo with insulin glargine (35.1 percent).
OK, what does Lilly say - use Trulicity with insulin for better results. We know the issue T2s have is not fasting insulin production by the pancreas but rather the meal time spikes so we know Lantus is not the proper tool. The proper tool is a meal time insulin and the best is the one which mimics the pancreas. Its really all about using the correct tool for the job. However, I bet if you use afrezza and properly dose and keep you meal time spike under 140 you won't need trulicity for BG control. In fact if all my early insulin studies are correct, early diagnosed T2 will see a regression in their T2 and will probably be able to control with no meds for years. I bet if the trial was done as trulicity/Lantus on one arm and only afrezza on the other, afrezza properly titrated would win hands down and trulicity would never have gotten approved.
Now, if your goal is weight loss and trulicity seems to help thats great but are there other methods which would provide similar or better weight-loss results without the risk? Whats clear is in the department of T2 glucose control and specifically the issue a T2 has which is meal time spikes trulicity has little effect. As Lilly says themselves after 28 weeks of treatment, Trulicity 1.5 mg plus insulin glargine significantly reduced A1C from baseline (1.44 percent) compared to placebo with insulin glargine (0.67 percent). Yes, less than 1% from the placebo is what Lilly says. https://investor.lilly.com/releasedetail.cfm?ReleaseID=975363 Thats not very good.