Purpose: The National Standards for Diabetes Self-Management Education and Support (DSMES) provide guidance and evidence-based, quality practice for all DSMES services. Due to the dynamic nature of health care and diabetes research, the National Standards are reviewed and revised approximately every 5 years by key stakeholders and experts within the diabetes care and education community. For each revision, the Task Force is charged with reviewing the current National Standards for appropriateness, relevance, and scientific basis and making updates based on current evidence and expert consensus. In 2021, the group was tasked with reducing administrative burden related to DSMES implementation across diverse care settings. Conclusion: The evidence supporting the 2022 National Standards clearly identifies the need to provide person-centered services that embrace cultural differences, social determinants of health, and the ever-increasing technological engagement platforms and systems. Payers are invited to review the National Standards as a tool to inform and modernize DSMES reimbursement requirements and to align with the evolving needs of people with diabetes (PWD) and physicians/other qualified health care professionals. The American Diabetes Association and the Association of Diabetes Care & Education Specialists strongly advocate for health equity to ensure all PWD have access to this critical service proven to improve outcomes both related to and beyond diabetes. The 2022 National Standards update is meant to be a universal document that is easy to understand and can be implemented by the entire health care community. DSMES teams in collaboration with primary care have been shown to be the most effective approach to overcome therapeutic inertia.

Tobacco use and secondhand tobacco-smoke (SHS) exposure are major national and international health concerns. Pediatricians and other clinicians who care for children are uniquely positioned to assist patients and families with tobacco-use prevention and treatment. Understanding the nature and extent of tobacco use and SHS exposure is an essential first step toward the goal of eliminating tobacco use and its consequences in the pediatric population. The next steps include counseling patients and family members to avoid SHS exposures or cease tobacco use; advocacy for policies that protect children from SHS exposure; and elimination of tobacco use in the media, public places, and homes. Three overarching principles of this policy can be identified: (1) there is no safe way to use tobacco; (2) there is no safe level or duration of exposure to SHS; and (3) the financial and political power of individuals, organizations, and government should be used to support tobacco control. Pediatricians are advised not to smoke or use tobacco; to make their homes, cars, and workplaces tobacco free; to consider tobacco control when making personal and professional decisions; to support and advocate for comprehensive tobacco control; and to advise parents and patients not to start using tobacco or to quit if they are already using tobacco. Prohibiting both tobacco advertising and the use of tobacco products in the media is recommended. Recommendations for eliminating SHS exposure and reducing tobacco use include attaining universal (1) smoke-free home, car, school, work, and play environments, both inside and outside, (2) treatment of tobacco use and dependence through employer, insurance, state, and federal supports, (3) implementation and enforcement of evidence-based tobacco-control measures in local, state, national, and international jurisdictions, and (4) financial and systems support for training in and research of effective ways to prevent and treat tobacco use and SHS exposure. Pediatricians, their staff and colleagues, and the American Academy of Pediatrics have key responsibilities in tobacco control to promote the health of children, adolescents, and young adults.

By the most recent estimates, 34.2 million people in the U.S. have diabetes (1). At the same time, 88 million people are at increased risk for developing type 2 diabetes. The U.S. also sees an increasing prevalence of both type 1 and type 2 diabetes in children and adolescents (2). Thus, more than 122 million Americans are at risk for developing devastating complications associated with chronic hyperglycemia (1). Diabetes self-management education and support (DSMES) is a critical element of care for all people with diabetes (PWD). "The purpose of DSMES is to give PWD the knowledge, skills, and confidence to accept responsibility for their self-management. This includes collaborating with their healthcare team, making informed decisions, solving problems, developing personal goals and action plans, and coping with emotions and life stresses" (3). DSMES interventions include activities that support PWD to implement and sustain the self-management behaviors and strategies to improve diabetes and related cardiometabolic conditions and quality of life on an ongoing basis. Despite progress in diabetes treatment modalities, glycemic and cardiometabolic outcomes continue to decline in the U.S. (4). Now, more than ever, the provision of DSMES is a vital component of the full treatment for diabetes.PWD are at risk for distress, life stress, and clinical depression, which can lead to poor health outcomes (5). The National Standards for Diabetes Self-Management Education and Support (hereinafter referred to as the National Standards) encourage the DSMES team to acknowledge and address the emotional burden of living with and managing diabetes-diabetes distress-and to consider the multitude of daily demands and decisions required of PWD, their families, and caregivers (6-9). To further illustrate, PWD generally visit their primary care physician (PCP)/other qualified healthcare professional two to four times per year, where the average appointment lasts 15-20 min and addresses four or more health conditions (10). This equates to the person with diabetes (PWD) spending less than 1% of their life with their healthcare professionals (10). Therefore, diabetes management decisions largely fall on PWD and/or caregivers, further highlighting the importance of increasing access to DSMES services that support ongoing self-management and decision making.The National Standards define timely, evidence-based, quality DSMES services that meet or exceed the Centers for Medicare & Medicaid Services quality standards. While the acronym DSMES is used in the literature and in current practice, it is important to note that the term diabetes self-management training (DSMT) is exclusively used when describing the Medicare benefit for diabetes self-management. The Medicare benefit for DSMT was established by the Balanced Budget Act (BBA) of 1997 with a final rule (65 FR 83130) published on 29 December 2000, implementing the BBA provisions and DSMT regulations (Title 42 of the Code of Federal Regulation sections 410.140 to 410.146). The DSMT benefit...

There is evidence in several cell systems suggesting that the GnRH receptor couples to multiple G proteins. Presently there are no published studies showing GnRH receptor coupling to Gialpha, Gsalpha, and Gq/11alpha in a single cell type. To examine this possibility we measured palmitoylation of G proteins in response to GnRH receptor occupancy, since this event is a measure of G-protein activation by cognate receptors. GnRH stimulated time (0-120 min)- and dose (10(-12)-10(-6) g/ml)-dependent palmitoylation of both Gialpha and Gsalpha. Palmitoylation is G-protein activation dependent; accordingly, pertussis toxin (100 ng/ml; PTX), phorbol myristic acid (100 ng/ml), and Antide (50 nM; a GnRH antagonist) did not stimulate palmitoylation of Gialpha or Gsalpha above basal levels. However, cholera toxin (5 microgram/ml), an activator of Gsalpha, stimulated palmitoylation of Gsalpha but not Gialpha. We used a lactotrope-derived cell line expressing the GnRH receptor (GGH3) to examine whether the ability of the receptor to couple multiple G proteins is gonadotroph specific. GGH3 cells were transfected with specific cDNA coding for different G proteins, and agonist-stimulated second messenger production was assessed. Buserelin (a GnRH agonist) stimulated increased cAMP release in Gsalpha cDNA-transfected GGH3 cells, whereas in Gialpha cDNA-transfected cells, both inositol phosphate (IP) production and cAMP release were decreased in response to buserelin. Transfection of Gqalpha, G11alpha, G14alpha, and G15alpha cDNA into GGH3 cells resulted in an increased IP production in response to buserelin, indicating that GnRH receptor couples to this PTX-insensitive G-protein family. The observations presented in this study provide evidence for GnRH receptor coupling to multiple G proteins in a single cell type.

The purpose of this study was to investigate the roles of androgenic and estrogenic mechanisms in the stimulation of structural growth and plasma GH in male puberty. To resolve these two possible mechanisms, we compared the effect of two androgens in the treatment of constitutional delay in growth and adolescence: an aromatizable androgen, testosterone (T), and a nonaromatizable androgen, dihydrotestosterone (DHT). Nine adolescent males, Tanner stage 1 or 2, were studied before and during treatment with T enanthate (group A) or DHT heptanoate (group B). After 2.5 months of treatment, the height velocity (HV) was 12.6 +/- 2.8 cm/yr (n = 3) in group A and 8.9 +/- 1.7 cm/yr (n = 6) in group B, both within the range of peak HV for pubertal males. In group A, the integrated concentration of GH (ICGH) increased from 3.12 +/- 0.90 to 13.67 +/- 6.0 micrograms/L (P < 0.05), and plasma insulin-like growth factor-I (IGFI) increased from 126.7 +/- 2.5 to 350.3 +/- 20.3 micrograms/L (P < 0.01); plasma T increased from 0.8 +/- 0.5 to 33.8 +/- 11.0 nmol/L (P < 0.001), and the LH response to LHRH decreased from 27.6 +/- 10.7 to 5.9 +/- 2.5 IU/L (P = NS). In group B, ICGH decreased from 4.32 +/- 0.61 to 2.39 +/- 0.42 (P < 0.025), and IGF-I decreased from 218.3 +/- 39.2 to 184.0 +/- 15.8 (P = NS). Plasma T increased from 2.0 +/- 0.5 to 2.7 +/- 0.8 (P = NS), and the LH response to LHRH decreased from 45.7 +/- 14.5 to 10.7 +/- 5.8 (P < 0.05). To further evaluate the mechanism of the effect of DHT on plasma GH, seven male subjects with adolescent gynecomastia were treated with DHT heptanoate, and their responses were studied at 1 week and 3.5 months. ICGH decreased in conjunction with a decrease in the integrated T concentration (r = -0.77; P < 0.001) and to a slight degree with decreasing plasma estradiol (r = -0.39; P < 0.2). Plasma IGF-I did not show a significant change in the subjects with gynecomastia. Thus, the increase in GH at puberty in males appears to be due to an estrogen-dependent mechanism. The suppressive effect of DHT on GH secretion may be due to either suppression of estradiol production or a direct effect. Acceleration of HV into the peak pubertal range by DHT without an increase in plasma GH suggests that an increase in GH is not necessary for the pubertal growth spurt.