First of all, don’t be afraid of insulin – its just another tool to control your diabetes, and will have less side effects than other treatments.
As to your question re worsening kidney function, I am not a MD, and can only explain it in the most hand-wavy of terms, but its essentially something similar that occurs in the retina of a diabetic, that causes capillary integrity to decrease and causes capillary collapse. The technical term is “diabetic kidney nephropathy”. You may want to head over to the American Diabetes Association Messageboards; there’s a bunch of very well-informed and knowledgeable people there who can answer your questions in far greater detail.
I’m surprised that your doctors recommend insulin for treatment of type II diabetes. Over here, doctors classify type II as “completly civilsation disease” brought on by bad habits (too much food - not only sugars, but overweight general and too little exercise) and can be cured 100% by changing those habits: loosing weight and exercising, and changing diet to healthier stuff. This is the preferred approach, and only if for complicating reasons that doesn’t work, meds are given to aid production.
I’ll second this - I was diagnosed 3 years ago, first as Type 2, then (6 month later when oral drug weren’t working) as Type 1. Insulin is a little scary at first, but honestly, after 3 years on it, I barely notice. Yeah, it’s more of a hassle than not being Insulin-dependent, but I can think of about a gazillion things that would be much, much worse. It’s not nearly as bad as it sounds.
That’s pretty much what they do in the US as well, but not everyone can make the necessary changes, or they do make the changes and they don’t work. I know at least thin, healthy-looking Type 2 who eats well and exercises, and is on Insulin, and I’ve talked to others in the same boat on the Internet.
Diet/Lifestyle changes work for a lot of Type 2s, but not everyone. And if it were me, given all the different Type 2 drugs on the market, I’d be looking at Insulin before a great many of them. It’s better understood, has a longer history, and is something a healthy body naturally produces - I like all those things WAY more than most of the alternative diabetes drugs.
Type 2 Diabetes is not completely “brought on by bad habits” nor can it “be cured 100% by changing those habits”. It is instead the result of both genetic and those environmental factors. Changing those habits, with intense lifestyle modifications, can result in substantially improved glycemic (blood sugar) control and decreased risk factors for heart disease (see the “Look AHEAD” trial) but will not “cure” the disease. It is an important aspect of treating the disease, in the very early phases may even be enough to achieve blood sugar goals, but, again, it does not cure it.
Type 2 Diabetes occurs as a result of both the loss of sensitivity of liver, muscle and fat cells to insulin and, at the same time, a poorer ability of the pancreas to effectively release the insulin. As the disease progresses the pancreas loses the cells that produce the insulin. The insulin resistance portion is pretty stable, but that progressive loss of pancreatic mass, that decline in the ability to produce adequate amounts insulin no matter how much the pancreas gets flogged, is what makes achieving the blood sugar goals harder and harder as the years go on.
That progression of the disease means that diet and exercise alone will rarely be enough to treat, as important of a component of care as they are. Medications almost always are needed as well. Non-insulin medications include some that increase the sensitivity of the cells to insulin, some that attempt to increase the production of insulin, some that attempt to decrease the absorption of glucose from the GI tract, and even some that effect other blood sugar related hormones (such as incretin). Initially just one of those will work but many times more than one is needed to achieve goals as the disease progresses and fairly often even several together are not enough.
Insulin however can always be dosed to work. And as Athena correctly notes: we know it well. Both the American Diabetic Association and the European Association for the Study of Diabetes now advise addng insulin fairly early.
Exactly. I am T1.5/LADA; my insulin dependence came on slowly, and I was first started on the meds that increase insulin production. It eventually (about a year and a half ago) got to the stage that I became completely insulin dependent (my doctors over tell me that I should have been on insulin years ago, as it would have preserved more of my pancreatic function, and I would have had better glycemic control), and like Athena, I barely notice it now. There are hassles, and things you have to watch out for, but once you learn about those (and there are some very very good books out there to help you), and know how to handle them, life can be about 95% normal.
So is the body responding to the specific type of sweetener at all, or is it simply the taste of sweetness? In other words, are different sorts of sweeteners likely to generate a different level of insulin response?
In regards to the cephalic phase insulin response, it is, as per the article cited in post #5, a function of the taste of sweetness stimulating taste receptors, both in the oral cavity and elsewhere. Different compounds stimulate those receptors differently and are likely to have different levels of insulin response but the shape of that response curve is apparently not known.
And also, for contanze, here is a link that give the joint ADA/European Association guidelines. (Not actually accessible in the abstract previously linked.)
Oh, more on both those points. That GLP-1 mentioned as one option, along with insulin, for Step 2, stands for glucagon-like peptide 1. It is an incretin, a set of hormones that seem to underlie the cephalic phase insulin response, at least as far as glucose is concerned. The duodenum has cells with sweet taste receptors that release GLP-1 in response to sweet stimuli (be it from glucose or an artificial sweetener, at least in vitro).
Note however that the artificial sweetener stimulating GP-1 release was documented in tissue culture. This recent study show that such might not occur all that readily in real humans ingesting an artificial sweetener.
Why are you concerned about the postprandial insulin response? It does not appear to cause obesity or insulin resistance, even though low-carbohydrate diets are effective at treating both of those conditions.
The effectiveness of low carb diets are predicated on the benefits from a lack of excessive insulin response, so any insulin response - from real blood glucose or not - is disruptive, from what I understand.