Eradicating Racism: An Endocrine Society Policy Perspective

The Endocrine Society recognizes racism as a root cause of the health disparities that affect racial/ethnic minority communities in the United States and throughout the world. In this policy perspective, we review the sources and impact of racism on endocrine health disparities and propose interventions aimed at promoting an equitable, diverse, and just healthcare system. Racism in the healthcare system perpetuates health disparities through unequal access and quality of health services, inadequate representation of health professionals from racial/ethnic minority groups, and the propagation of the erroneous belief that socially constructed racial/ethnic groups constitute genetically and biologically distinct populations. Unequal care, particularly for common endocrine diseases such as diabetes, obesity, osteoporosis, and thyroid disease, results in high morbidity and mortality for individuals from racial/ethnic minority groups, leading to a high socioeconomic burden on minority communities and all members of our society. As health professionals, researchers, educators, and leaders, we have a responsibility to take action to eradicate racism from the healthcare system. Achieving this goal would result in high-quality health care services that are accessible to all, diverse workforces that are representative of the communities we serve, inclusive and equitable workplaces and educational settings that foster collaborative teamwork, and research systems that ensure that scientific advancements benefit all members of our society. The Endocrine Society will continue to prioritize and invest resources in a multifaceted approach to eradicate racism, focused on educating and engaging current and future health professionals, teachers, researchers, policy makers, and leaders.

Practical Guidelines for Diagnosing and Treating Thyroid Disease Based on the WOMED Metabolic Model of Disease Focusing on Glycolysis and Coenzyme Q10 Deficiency—A Clinical Alternative to the 2021 Retired Clinical Practice Guidelines of the Endocrine Society

This review aims to provide a functional, metabolic view of the pathogenesis of benign thyroid disease. Here, we summarize the features of our previous publications on the “WOMED model of benign thyroid disease”. As of 2021, the current state of art indicates that the basic alteration in benign thyroid disease is a metabolic switch to glycolysis, which can be recognized using 3D-power Doppler ultrasound. A specific perfusion pattern showing enlarged vessels can be found using this technology. This switch originates from an altered function of Complex I due to acquired coenzyme Q10 deficiency, which leads to a glycolytic state of metabolism together with increased angiogenesis. Implementing a combined supplementation strategy that includes magnesium, selenium, and CoQ10, the morphological and perfusion changes of the thyroid can be reverted, i.e., the metabolic state returns to oxidative phosphorylation. Normalization of iron levels when ferritin is lower than 50 ng/mL is also imperative. We propose that a modern investigation of probable thyroid disease requires the use of 3D-power Doppler sonography to recognize the true metabolic situation of the gland. Blood levels of magnesium, selenium, CoQ10, and ferritin should be monitored. Thyroid function tests are complementary so that hypo- or hyperthyroidism can be recognized. Single TSH determinations do not reflect the glycolytic state.

Hypoglycemia screening of asymptomatic newborns on the 2nd day of life

BACKGROUND: Neonatal hypoglycemia management in the first 48 hours is guided by the American Academy of Pediatrics (AAP) and Pediatric Endocrine Society (PES) recommendations. Our aim was to determine the incidence of hypoglycemia via point of care test (POCT) on the 2nd day of life (DOL) among healthy, asymptomatic neonates regardless of risk factors. METHODS: In this prospective observational study, preprandial point of care glucose concentration was measured on the 2nd DOL in 150 healthy, asymptomatic neonates in the newborn nursery. We used 50 mg/dl (2.8 mmol/L) as the hypoglycemia threshold based on PES recommendations. RESULTS: The incidence of hypoglycemia on the second DOL was 10% among asymptomatic neonates (no risk factors = 8% ; late preterm birth (LPT) + small for gestational age (SGA) = 16% ; large for gestational age (LGA) + infant of diabetic mother (IDM) = 6%). SGA + LPT neonates accounted for the majority of the hypoglycemic cases (53.3%) and exhibited a trend towards the lowest glucose concentration (p = 0.09). CONCLUSION: The incidence of hypoglycemia on DOL 2 among asymptomatic neonates is high and of unclear significance in the absence of dedicated neurodevelopmental follow-up.

Use of Thyroid Hormones in Hypothyroid and Euthyroid Patients: A 2020 THESIS Questionnaire Survey of Members of the Swedish Endocrine Society

BackgroundThe standard treatment of hypothyroidism is levothyroxine (LT-4). However, there are several controversies regarding treatment of hypothyroid patients.AimTo investigate the Swedish endocrinologists’ use of thyroid hormones in hypothyroid and euthyroid individuals.MethodsPhysician members of the Swedish Endocrine Society (SEF) were invited by e-mail to participate in an online survey investigating this topic.ResultsOut of the eligible 411 members, 116 (28.2%) responded. The majority (98.9%) stated that L-T4 is the treatment of choice. However, around 50% also prescribed liothyronine (L-T3) or a combination of L-T4+L-T3 in their practice. Combination therapy was mostly (78.5%) used in patients with persistent hypothyroid symptoms despite biochemical euthyroidism on L-T4 treatment. Most respondents prescribed L-T4 tablets and did not expect any major changes with alternative formulations such as soft-gel capsules or liquid formulations in situations influencing the bioavailability of L-T4. In euthyroid patients, 49.5% replied that treatment with thyroid hormones was never indicated, while 47.3% would consider L-T4 for euthyroid infertile women with high thyroid peroxidase (TPO) antibody levels.ConclusionThe treatment of choice for hypothyroidism in Sweden is L-T4 tablets. Combination therapy with L-T4+L-T3 tablets was considered for patients with persistent symptoms despite biochemical euthyroidism. Soft-gel capsules and liquid solutions of L-T4 were infrequently prescribed. Swedish endocrinologists’ deviation from endocrine society guidelines merits further study.

Vitamin D dosage

Despite its historical name, vitamin D is not a vitamin at all but a hormone that, when activated, is a metabolically active steroid fat-soluble hormone that acts on cellular receptors. Vitamin D hormone is synthesized endogenously and then metabolized in the body, provi-ding that there are the necessary precursors and some factors — the effects of ultraviolet light on the skin. At the same time, vitamins themselves are nutrients, co-factors of biochemical reactions that are not synthesized in the body and cannot interact with receptors, consumed with food, so the hormone D is not a vitamin. Disputes about its use and dosage continue throughout the study period of vitamin D hormone. Most reputable experts in Europe and the USA support the need to replenish and maintain a normal level of vitamin D, believing it to be completely safe and useful. In 2011, the US Endocrine Society issued clinical practice guidelines for vitamin D, indicating that the desired serum concentration of 25(OH)D is > 75 nmol/l (> 30 ng/ml) to achieve the maximum effect of this vitamin on calcium metabolism, bone, and muscle metabolism. According to them, for a consistent increase in serum 25(OH)D above 75 nmol/l (30 ng/ml), adults may require at least 1,500-2,000 IU/day of additional vitamin D, at least 1,000 IU/day in children and adolescents. The most common form of thyroid dysfunction is secondary hyperparathyroidism, which develops due to vitamin D defect/deficiency (80–90 %). Non-optimal serum concentrations of 25(OH)D lead to secondary hyperparathyroidism, potentially leading to decreased bone mineralization and, ultimately, to an increased risk of osteopenia, osteoporosis and fractures, cardiac arrhythmia, and increased blood pressure. Vitamin D is most commonly used at a star-ting dose of 5,000 IU daily for 2–3 months, then transferring patients to maintenance doses of 2,000–4,000 IU/day daily that are consi-dered safe. However, it should be noted that some patients will need constant administration of 5,000 IU of vitamin D per day for a long time (years) to maintain the target optimal level of 25(OH)D in the blood, especially in patients with normocalcemic forms of secondary hyperparathyroidism.