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Atherosclerosis is the world’s leading cause of death [1]. Much, but not all, is known about atherosclerosis development. Classical modifiable risk factors include diabetes mellitus, hypertension, hyperlipidemia, and smoking, while other important risk factors include abdominal obesity, excessive alcohol intake, lack of fruit and vegetable intake, and psychosocial factors [2]. The suggestion that thyroid function may be related to atherosclerosis is not new [3]. There is general agreement that overt hypothyroidism promotes cardiovascular disease, including atherosclerosis. Mechanisms through which decreased thyroid hormone concentrations lead to atherosclerosis include elevated low-density lipoprotein cholesterol, diastolic hypertension, heightened coagulability, and actions on vascular smooth muscle [3]. However, much debate continues whether subclinical hypothyroidism similarly leads to increased cardiovascular events. A very large meta-analysis of previous studies suggested modestly increased risk with subclinical hypothyroidism [4], although there was significant heterogeneity of the results among the studies included. The meta-analysis also found that by age, the youngest patients had the most positive hazard ratio estimate, but statistical significance was not reached, likely because of small subgroup numbers [4]. Interestingly, a recent paper reported increased cardiovascular events in younger (B70 years) but not older ([70 years) patients with subclinical hypothyroidism [5]. This is interesting because subclinical hypothyroidism in some older individuals may not be pathologic, and is less likely to be due to autoimmune thyroid disease [6]. Some authors hypothesize that autoimmune thyroid disease per se may play a role in atherosclerosis development. Biochemically, it has been reported that Hashimoto’s thyroiditis causing subclinical hypothyroidism is associated with low-grade inflammation as measured by high-sensitivity C-reactive protein and interleukin-6 levels, and is linked to endothelial dysfunction [7]. That systemic lowgrade inflammation has been demonstrated in Hashimoto’s thyroiditis is not surprising given that peripheral (as opposed to simply intra-thyroidal) activation of the immune system in Hashimoto’s thyroiditis patients has also been reported [8]. At the organ level, another report showed that arterial stiffness, but not carotid intima-medial thickness (CIMT), was increased in euthyroid Hashimoto’s thyroiditis patients compared to controls [9]. Ciccone et al. [10] investigated overweight and obese euthyroid patients, finding that CIMT was indeed increased in patients with Hashimoto’s thyroiditis, compared to those without. At the population level, in a retrospective study, Nyirenda et al. [11] found that Scottish patients with Hashimoto’s thyroiditis over (but not under) the age of 50 years had more hospitalizations for cardiovascular disease than controls. Furthermore, using nationwide Swedish linked data registries, Zoller et al. [12] recently reported that patients hospitalized with Hashimoto’s thyroiditis (and numerous other autoimmune disorders) subsequently had higher rates of coronary heart disease and stroke [13]. In this issue of Endocrine, Topaloglu et al. [14] add further evidence to the debate. This study recruited 48 euthyroid premenopaual women with Hashimoto’s thyroiditis and compared them to 18 controls with respect to D. S. A. McLeod (&) Cancer Control Group, Queensland Institute of Medical Research, Herston, QLD 4029, Australia e-mail: donald.mcleod@qimr.edu.au

The thyroid gland is the most common organ affected by autoimmune disease. Other autoimmune diseases, most notably type 1 diabetes mellitus, are increasing in incidence. It is unknown whether autoimmune thyroid diseases are following the same pattern. This review summarizes studies of autoimmune thyroid disease incidence and prevalence since 1950, not only for these measures of occurrences, but also for commenting on identified risk factors for thyroid autoimmunity. We find that incidence of autoimmune thyroid disease is currently higher than in historic series although the studies are so variable in design, patient population, disease definition, and laboratory methods that it is impossible to tell whether this difference is real. Further research is required to assess the possibility of changing disease patterns of autoimmune thyroid disease as opposed to simple changes in diagnostic thresholds.