Leave it to Anne Peters MD to be co-editor of this amazing resource for medical providers who treat patients with Type 1 diabetes (Type 1 Diabetes Sourcebook, 2013. Anne Peters, MD, and Lori Laffel, MD, MPH, Editors. JDRF and American Diabetes Association). The book is written for the Type 1 medical community, but I think it has a lot of good information for the patient with Type 1 diabetes. Unlike so many books on Type 1 diabetes that only focus on kids, this one addresses both children AND adults with Type 1 diabetes, and notes that adults represent 85% of the Type 1 population. I also appreciate the level of compassion shown in the book towards those with T1D—in particular, I am so unused to compassion expressed towards people with adult-onset Type 1 diabetes, but this excellent book has it in abundance. Here are direct-quote gems that I found in The Type 1 Diabetes Sourcebook (keeping in mind that my usual focus is adult-onset Type 1 diabetes):
• There is no authoritative source for the incidence of T1D in adults in the U.S. population. However, it is important to note that T1D is not a childhood disease and may be diagnosed into adulthood with an additional peak in the sixth and seventh decades of life [emphasis mine]. Page 1.
• Recent data are needed regarding the incidence of T1D in adults. Notably, nearly 85% of people living with Type 1 diabetes are adults. Page 8.
• 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.
• 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.
• We want [medical] providers to know that patients with T1D are not the same as patients with T2D; thus, we describe the specific approaches for patents with T1D across the life span. Page 73.
• The pathophysiology of the two diseases [T1D and T2D] differ on a basic pathophysiologic level such that T1D is marked by insulinopenia while T2D is characterized by obesity, hyperinsulinemia, insulin resistance, and relative insulinopenia. Page 104.
• Regarding diagnostic criteria (ADA, WHO): As the ADA/WHO diagnostic criteria are heavily influenced by the overwhelming burden of T2D worldwide, clinicians must recall that these criteria are not T1D specific and do not always provide optimal sensitivity for the diagnosis of T1D. ADA and WHO criteria are used to broadly diagnose diabetes, however, a combination of immunologic, genetic, and phenotypic features must be used to differentiate among the different forms of diabetes. Page 4 and 5.
• We consider all patients with evidence of autoimmunity to have T1D. Page 5.
• Given the tremendous burden T2D places on the U.S. health care system, it is not surprising that patients, health care providers, and researchers often use the nonspecific term diabetes when referring to T2D. However, the practice of referring to T2D as simply diabetes cultivates numerous dangerous misconceptions regarding the etiology, pathophysiology, and treatment of other subtypes of diabetes [emphasis mine]. Page 6.
• Despite the historical focus on children when discussing the epidemiology of T1D, it is critical to consider that adults make up 25-50% of newly diagnosed patients and represent the overwhelming majority of patients living with T1D. Importantly, adults with LADA may represent an additional 10% of those adults incorrectly diagnosed with T2D. As these patients are far more likely to progress rapidly to requiring insulin therapy, clinicians treating adults must be aware of the need to screen for LADA, particularly in their patients with relatively low BMI. [Elsewhere in the book, on page 24, the authors state that 60% of new-onset T1D is seen in adults, and that is confirmed by the most recently available data from the CDC.]
• [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.
• It is often unappreciated that many individuals with T1D will have significant amounts of C-peptide, representing residual beta cell function. The standard teaching that T1D is defined as complete absence of beta cells is inaccurate and is a disservice to both patients and providers. Among 411 participants in the Joslin Medalists study (those with T1D greater than or equal to 50 years), 67.4% still had detectable C-peptide. Pages 26 and 27.
• 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.
• 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.
• Recent data are needed regarding the incidence of T1D in adults. Notably, nearly 85% of people living with Type 1 diabetes are adults. Page 8.
• 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.
• 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.
• We want [medical] providers to know that patients with T1D are not the same as patients with T2D; thus, we describe the specific approaches for patents with T1D across the life span. Page 73.
• The pathophysiology of the two diseases [T1D and T2D] differ on a basic pathophysiologic level such that T1D is marked by insulinopenia while T2D is characterized by obesity, hyperinsulinemia, insulin resistance, and relative insulinopenia. Page 104.
• Regarding diagnostic criteria (ADA, WHO): As the ADA/WHO diagnostic criteria are heavily influenced by the overwhelming burden of T2D worldwide, clinicians must recall that these criteria are not T1D specific and do not always provide optimal sensitivity for the diagnosis of T1D. ADA and WHO criteria are used to broadly diagnose diabetes, however, a combination of immunologic, genetic, and phenotypic features must be used to differentiate among the different forms of diabetes. Page 4 and 5.
• We consider all patients with evidence of autoimmunity to have T1D. Page 5.
• Given the tremendous burden T2D places on the U.S. health care system, it is not surprising that patients, health care providers, and researchers often use the nonspecific term diabetes when referring to T2D. However, the practice of referring to T2D as simply diabetes cultivates numerous dangerous misconceptions regarding the etiology, pathophysiology, and treatment of other subtypes of diabetes [emphasis mine]. Page 6.
• Despite the historical focus on children when discussing the epidemiology of T1D, it is critical to consider that adults make up 25-50% of newly diagnosed patients and represent the overwhelming majority of patients living with T1D. Importantly, adults with LADA may represent an additional 10% of those adults incorrectly diagnosed with T2D. As these patients are far more likely to progress rapidly to requiring insulin therapy, clinicians treating adults must be aware of the need to screen for LADA, particularly in their patients with relatively low BMI. [Elsewhere in the book, on page 24, the authors state that 60% of new-onset T1D is seen in adults, and that is confirmed by the most recently available data from the CDC.]
• [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.
• It is often unappreciated that many individuals with T1D will have significant amounts of C-peptide, representing residual beta cell function. The standard teaching that T1D is defined as complete absence of beta cells is inaccurate and is a disservice to both patients and providers. Among 411 participants in the Joslin Medalists study (those with T1D greater than or equal to 50 years), 67.4% still had detectable C-peptide. Pages 26 and 27.
• 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.
• 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.
Originally published at Tudiabetes.org
