The Type 1 Diabetes Sourcebook (2013: Anne Peters, MD, and Lori Laffel, MD, MPH, Editors (JDRF and American Diabetes Association)) has some excellent recommendations for new-onset Type 1 in adults, much of which I summarized in this blog. Here is information that may be of use to you, Krisa:
1) Adults developing T1D may follow a less precipitous course with few or no symptoms and an elevated glucose level identified incidentally on routine blood work. These individuals may be treated (unsuccessfully) with oral agents before it is determined that they are actually patients with evolving T1D who need treatment with insulin [emphasis mine]. Page 3.
2) Initial Treatment for Adults: Adult patients can vary greatly at presentation, from a more acute picture, with DKA and marked hyperglycemia, to a more gradual course such as is often seen in LADA. For those presenting acutely as well as those presenting more indolently, starting insulin is the mainstay of therapy [emphasis mine]. Page 79.
3) [In persons with LADA], failure to control glucose [with non-insulin therapies for T2D] should rapidly lead to insulin therapy rather than allowing months to years of experimenting with non-insulin approaches [emphasis mine]. Page 24.
4) For those with early T1D, expert opinion (i.e., not data driven) recommends either low doses of basal insulin to prevent DKA or prandial insulin to prevent postprandial hyperglycemia. Page 27.
5) Preservation trials focus on halting further pancreatic beta cell destruction after T1D diagnosis. At the time of diagnosis, it has been estimated that 15-40% of beta cell function remains. This remnant can serve one well while it lasts, as evidenced by better overall glycemic control during this remission or honeymoon phase, with lower A1Cs, less glycemic variability, and less hypoglycemia risk. Page 42.
Here is a footnote from my Bill of Rights blog: In the Diabetes Control and Complications Trial (DCCT), all subjects with adult-onset Type 1 diabetes had some residual beta cell function (Bernard Zinman MD, DCCT). Those who were assigned to the intensive insulin therapy group were slower to lose residual beta cell function than the conventional therapy group (risk reduction 57%). Clearly, early intensive insulin therapy has enormous benefit. As demonstrated in the DCCT, “intensive therapy for Type 1 diabetes helps sustain endogenous insulin secretion, which, in turn, is associated with better metabolic control and lower risk for hyperglycemia and chronic complications.” LADA researchers in Japan (Kobayashi et al, 2002) have conclusively demonstrated that better preservation of beta cell function occurs with exogenous insulin compared to sulfonylureas, and that sulfonylureas hasten beta cell destruction. In other words, doctors may inappropriately use Type 2 therapies in new-onset Type 1 diabetes, but all scientific studies indicate that the correct therapy is intensive insulin therapy.