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In healthy older people the metabolism of thyroid hormones is physiologically altered and can possibly even actively contribute to longevity. This should also be taken into consideration in the treatment of diseases of the thyroid and principally also for younger patients. For example, with progressing age comorbidities become more prevalent and especially in cardiovascular diseases, hyperthyroidism is less well tolerated, and should be treated more aggressively. Benign multinodular goiter also becomes more prevalent in old age and should be surgically treated when causing mechanical symptoms. The treatment concept for malignant diseases should be adapted to the holistic situation of the patient but principally in the same manner as in younger patients. Old and very old patients also benefit from adequate, risk-adapted treatment of thyroid gland diseases so that appropriate diagnostics and clarification are meaningful, regardless of age.

In recent years, there has been worldwide a significant (relative) increase in "small" thyroid cancer (pT1 = tumor size of ≤10 mm), which has now reached a plateau. This fact and the absence of prospective and randomized clinical trials are increasingly leading to a discussion of the so-called risk-adapted management of differentiated thyroid cancer. The available studies are partly incomplete, retrospective and difficult to compare. In addition, factors such as different iodine supply, cost-benefit considerations and regional differences in quality of surgical procedures influence the implementation of therapy concepts. Therefore, the therapy of the differentiated thyroid cancer is currently the subject of intensive discussion, especially in "low risk" situations. There is a worldwide trend to classify the risk of differentiated thyroid cancer in general lower than in the past and thus also to reduce the extent of the traditionally recommended therapy. The discussion is increasingly moving from the "one size fits all" towards personalized and thus risk-adapted therapy of the differentiated thyroid cancer.The main goal of this "paradigm shift" is to avoid an "overtreatment" which may be associated with permanent complications due to "unnecessary" surgical procedures and any negative effects of radioiodine ablation.This overview attempts to answer the following questions: When is a risk-adapted therapy for differentiated thyroid cancer justified? What are the consequences in differentiated thyroid cancer if no radioiodine therapy is performed?

Background: We aimed to study the validity of six published ultrasound criteria for risk stratification of thyroid nodules in the former severely iodine deficient population of Austria., Methods: Retrospective, single centre, observer blinded study design. All patients with a history of thyroidectomy due to nodules seen in the centre between 2004 and 2014 with preoperative in-house sonography and documented postoperative histology were analyzed ( n  = 195). A board of five experienced thyroidologists evaluated the images of 45 papillary carcinomas, 8 follicular carcinomas, and 142 benign nodules regarding the following criteria: mild hypoechogenicity, marked hypoechogenicity, microlobulated or irregular margins, microcalcifications, taller than wide shape, missing thin halo., Results: All criteria but mild hypoechogenicity were significantly more frequent in thyroid cancer than in benign nodules. The number of positive criteria was significantly higher in cancer (2.79 ± 1.35) than in benign nodules (1.73 ± 1.18; p  < 0.001). Thus, with a cut-off of two or more positive criteria, a sensitivity of 85% and a specificity of 45% were reached to predict malignancy in this sample of thyroid nodules. As expected, the findings were even more pronounced in papillary cancer only (2.98 ± 1.32 vs. 1.73 ± 1.18, p  < 0.001). The six ultrasound criteria could not identify follicular cancer., Conclusion: Our findings support the recently published EU-TIRADS score. Apart from mild hypoechogenicity, the analyzed ultrasound criteria can be applied for risk stratification of thyroid nodules in the previously severely iodine deficient population of Austria., Competing Interests: The ethic committee of the Medical University of Vienna approved this study which did not involve direct patient care. (1461/2015).All authors gave their approval for the final version to be published and agree to be accountable for this work.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Objective: Growth differentiation factor 15 (GDF15) is a cardiovascular biomarker belonging to the transforming growth factor-β superfamily. Increased GDF15 concentrations are associated with insulin resistance, diabetes and obesity. We investigated the physiological effects of meal composition and obesity on the regulation of systemic GDF15 levels., Design: Lean (n = 8) and obese (n = 8) individuals received a carbohydrate- or fat-rich meal, a 75 g oral glucose load (OGTT) or short-term fasting. OGTTs were performed in severely obese patients (n = 6) pre- and post-bariatric surgery., Methods: Circulating serum GDF15 concentrations were studied in lean and obese individuals in response to different meals, OGTT or short-term fasting, and in severely obese patients pre- and post-bariatric surgery. Regulation of GDF15 mRNA levels and protein release were evaluated in the human hepatic cell line HepG2., Results: GDF15 concentrations steadily decrease during short-term fasting in lean and obese individuals. Carbohydrate- and fat-rich meals do not influence GDF15, whereas an OGTT leads to a late increase in GDF15 levels. The positive effect of OGTT on GDF15 levels is also preserved in severely obese patients, pre- and post-bariatric surgery. We further studied the regulation of GDF15 mRNA levels and protein release in HepG2, finding that glucose and insulin independently stimulate both GDF15 transcription and secretion., Conclusion: In summary, high glucose and insulin peaks upregulate GDF15 transcription and release. The nutrient-induced increase in GDF15 levels depends on rapid glucose and insulin excursions following fast-digesting carbohydrates, but not on the amount of calories taken in., (© 2016 European Society of Endocrinology.)