Background: Numerous studies have evaluated the effect that mindfulness-based interventions (MBIs) have on multiple health outcomes. For its part, stress is a natural response to environmental disturbances and within the associated metabolic responses, alterations in cortisol levels and their measurement in different tissues are a way to determine the stress state of an individual. Therefore, it has been proposed that MBIs can modify cortisol levels. Methods and results: The objective of this systematic review was to analyze and summarize the different studies that have evaluated the effect of MBIs on cortisol levels. The following databases were consulted: MEDLINE, AMED, CINAHL, Web of Science, Science Direct, PsycINFO, SocINDEX, PubMed, the Cochrane Library and Scopus. The search terms “mindfulness”, “mindfulness-based interventions” and “cortisol” were used (and the search was limited to studies from January 1990 to May 2024). In order to reduce selection bias, each article was scrutinized using the JBI Critical Appraisal Checklist independently by two authors. We included those studies with specified intervention groups with at least one control group and excluded duplicate studies or those in which the intervention or control group was not adequately specified. Significant changes in cortisol following MBIs were found in 25 studies, while 10 found no changes. The small sample size, lack of randomization, blinding, and probable confounding and interaction variables stand out in these studies. Conclusion: MBIs have biological plausibility as a means of explaining a positive effect on cortisol levels; however, the weakness of the studies and the absence of robust designs makes it difficult to establish a causal association between both variables. Registration number: INPLASY2024110017.

Background: Hashimoto’s thyroiditis (HT) is the most common autoimmune thyroid disease (AITD) and is characterized by the presence of thyroid autoantibodies against thyroid peroxidase and/or thyroglobulin. Several studies have found that the global prevalence of HT has increased in recent decades, while others show the opposite. Methods and Results: The objective of this scoping review was to synthesize and analyze the different studies that have evaluated the prevalence of HT (in adults) and the possible associated factors. The following databases were consulted, as follows: MEDLINE, Web of Science, PubMed, and Scopus. The search terms “epidemiology”, “prevalence”, and “Hashimoto disease” and “Hashimoto thyroiditis” were used. The search was limited to articles published between January 1965 and October 2024, and only articles in English were considered. In order to reduce selection bias, each article was scrutinized using the JBI Critical Appraisal Checklist independently by two authors. Studies were included if the number of participants (study population and/or cases and controls, depending on the study design) was clearly described and duplicate studies were excluded. A total of 59 studies were identified, the vast majority of them used a cross-sectional design, using different methods of disease assessment. Conclusions: Globally, the prevalence of HT is estimated to be between 5–10%; some areas with prevalences > 20% and others < 0.5% were identified. Prevalence is also higher in women than in men. Multiple underlying factors (genetic, epigenetic, environmental, and lifestyle), together with socioeconomic, nutritional, overdiagnosis, inter alia, may explain (at least in part) the wide variability in the prevalence of HT.

Vitamin B12 (B12) is necessary for the proper functioning of the central and peripheral nervous systems. Although there is no exact definition for B12 levels, a value of 200 pg/mL is compatible with deficiency, 200–299 pg/mL is considered borderline, and 300 pg/mL is considered normal. In population studies, the prevalence of B12 deficiency ranges between 2.9% and 35%. Furthermore, many medications, such as metformin [for type 2 diabetes mellitus (T2DM)], can cause B12 deficiency. The objectives of this study were to determine the population status of B12 in southwestern Colombia (and the status of B12 in subjects with T2DM). In the total population (participants with and without T2DM), the prevalence of B12 deficiency was 17.8%; that of borderline was 19.3%; and that of normal levels was 62.9%. The prevalence of deficiency increased with age and was significantly higher in those aged ≥60 years (p = 0.000). In T2DM subjects, the prevalence of deficiency was significantly higher concerning those without T2DM (p = 0.002) and was significantly higher in those who received >1 gm/day of metformin (p = 0.001). Thus, the prevalence of deficiency and borderline levels of B12 in our population was high, particularly in those >60 years of age. B12 deficiency was significantly higher in individuals with T2DM than in individuals without T2DM, especially among those receiving high doses of metformin.

Population zinc and iron status appear to be associated with an increased risk of thyroid function abnormalities and thyroid autoimmunity (AITD). In the present study, we aimed to determine whether zinc and/or iron levels (assessed by ferritin levels) were associated with the presence of AITD and with alterations in thyroid function. A population-based case–control study (n = 1048) was conducted (cases: n = 524; controls: n = 524). Participants were measured for blood concentrations of zinc and ferritin, TSH, FT4, FT3, and thyroid autoantibodies. No significant differences were found in relation to ferritin levels between cases and controls. Among cases, the prevalence of low zinc levels in those with hypothyroidism (both subclinical and overt) was 49.1% [odds ratio (OR) of low zinc levels: 5.926; 95% CI: 3.756–9.351]. The prevalence of low zinc levels in participants with hyperthyroidism (both subclinical and overt) was 37.5% [OR of low zinc levels: 3.683; 95% CI: 1.628–8.33]. The zinc value that best discriminated the highest frequency of AITD was 70.4 µg/dL [sensitivity: 0.947, 1–specificity: 0.655, specificity: 0.345]. The highest frequency of AITD was calculated based on a zinc value <70 µg/dL (relative to a normal value), with this frequency being significantly higher in cases than in controls [OR: 9.3; 95% CI: 6.1–14.3 (p = 0.001)]. In conclusion, the results of our study suggest that zinc deficiency is associated with an increased frequency of functional thyroid disorders and thyroid autoimmunity.

Background: The population prevalence of functional alterations and thyroid autoimmunity is high, and numerous genetic and environmental aspects have been described as triggering factors. Objectives: The objective of this study was to determine the prevalence of functional alterations and thyroid autoimmunity in an urban population of Colombia. Materials and methods: It is a cross-sectional, population-based study (n= 9,638) conducted on an urban population of Popayán-Cauca-Colombia between February 5th, 2018, to December 11th, 2021. The variables evaluated were thyrotropin (TSH), free T4 (FT4), and anti-thyroid antibodies (thyroid peroxidase antibodies: TPOAb, and thyroglobulin antibodies: TgAb). Results: TSH in men was significantly higher than in women. No differences were observed in the values of FT4, TPOAb, and TgAb (according to sex). The prevalence of normal thyroid function and subclinical hypothyroidism was significantly higher in men. The positivity of TPOAb and TgAb was 22.3% and 19.2%, respectively. TSH levels increased with age (both in men and in women). In participants with normal FT4 and negative TPOAb, the TSH was significantly higher. TSH was significantly higher in TPOAb-positive individuals and among those with TPOAb and TgAb positives, as well as in women with positive TPOAb and men with positive TPOAb and TgAb. Conclusion: In an urban population of Colombia, TSH was found to be higher than in populations of other geographical areas, especially in older individuals and in the presence of positive anti-thyroid antibodies, a high prevalence of functional alterations and thyroid autoimmunity was also found. These findings can be explained by excess iodine consumption and some environmental factors.

Background: Hashimoto’s thyroiditis (HT) is characterized by the loss of tolerance to thyroid autoantigens [thyroid peroxidase (TPO) and thyroglobulin (Tg)], usually identifying circulating antibodies (Abs) against these thyroid autoantigens (TPOAb and/or TgAb), together with a significant lymphocytic infiltration, causing an increased risk of hypothyroidism. Among the multiple mechanisms described for the development of HT is the nutritional status of several micronutrients, including iodine. Iodine deficiency or excess is associated with thyroid function disorders and, likely, thyroid autoimmunity. Thus, iodized salt intake [especially through universal salt iodization (USI) programs] may be influencing the prevalence of HT. The objectives of this systematic review are to describe and analyze changes over time in the prevalence of HT following the implementation of USI programs. Methods and results: The following databases were consulted for articles published from January 1965 to January 2025: Pubmed/Medline; ProQuest; Scopus; Biosis; Web of Science; and Google Scholar. The search terms were as follows: “iodine”, “salt”, “intake”, “prevalence”, AND Hashimoto’s thyroiditis. Only English language articles were taken into account, and each of them was scrutinized according to the JBI Critical Appraisal Checklist. Only those studies in which the design, study population, number of participants, country, evaluation post-USI (years), and the prevalence of thyroid Abs positivity were described were included. In total, 74 studies were identified, of which 31 evaluated thyroid Abs values post-USI. Conclusions: Excess iodine intake, mediated by USI programs without an adequate follow-up and monitoring plan, may explain (at least in part) the prevalence and distribution of HT; therefore, it is a real challenge to establish a balance between healthy salt intake, USI program strategies, and possible functional outcomes and thyroid autoimmunity in the population. Registration number: INPLASY202540074.