Iodine - again!
My reading of this suggests that, in the general population, we want to see relatively high selenium levels.
And, in particular, we want that state before any increase in iodine levels - whether from diet, iodised salt or other sources. We might find that this state needs to be achieved for a long time.
This paper says absolutely NOTHING about the advisability or otherwise of selenium and iodised salt in those who already have thyroid autoimmunity issues.
Selenium intake was categorised as:
Lowest = T1 (<88.95 µg)
Medium = T2 (88.95~133.60 µg)
Highest = T3 (≥133.60 µg)
Note that the paper says:
A high selenium intake can protect the thyroid from autoimmune damage caused by excessive iodine.
It does not say that a high selenium intake is essential in other circumstances.
And my final note: Excess selenium is itself bad for us. What constitutes excess for individuals is very difficult without being tested. We simply do not know the selenium content of the foods we, as individuals, consume. Advice is usually to keep supplementation to no more than 100 micrograms a day except for short-term use in some specific cases. Given that supplements are on top of dietary intake, I'd even suggest a lower dose might be plenty for a lot of people.
The Relationships among the Urinary Iodine Concentration, Selenium Intake, and Thyroid Antibodies in Adults, Including the Interaction between Iodine and Selenium: National Health and Nutrition Examination Survey 2007–2012
Abstract
Objectives: The objective of this study was to examine the urinary iodine concentration (UIC)–thyroid autoimmunity (TAI) association and UIC–selenium intake interaction in U.S. adults. Methods: We analyzed 2007–2012 National Health and Nutrition Examination Survey (NHANES) data on ≥20-year-old adults (n = 6612). Their food and supplemental selenium intake was measured. The associations of the UIC and selenium intake with thyroid peroxidase antibody (TPOAb) positivity, thyroglobulin antibody (TgAb) positivity, and TAI were assessed via weighted multivariable logistic regression. Interaction and subgroup analyses were conducted. Nonlinear relationships were explored and visualized via restricted cubic splines (RCSs). Results: Compared with a UIC 100~200 μg/L, a UIC 500~800 μg/L was associated with a 57% increased TPOAb positivity risk (OR = 1.57 [CI = 1.07–2.30]; p = 0.022), a one-fold greater TgAb positivity risk (OR = 2.00 [CI = 1.10–3.65]; p = 0.025), and a 62% increased TAI risk (OR = 1.62 [CI = 1.07–2.45]; p = 0.024). Nonlinear relationships between the UIC and thyroid antibody positivity were observed. According to the univariate models, each 1 μg increase in selenium intake was associated with a 0.049 IU/mL decrease in the TPOAb levels (β [95% CI] = −0.049 [−0.092–−0.005]; p = 0.028). In the low-selenium group, a UIC of 200~300 μg/L was a risk factor for TPOAb positivity (p = 0.046). At a moderate level of selenium intake, a UIC of 300~800 μg/L significantly increased the TPOAb positivity risk (all p 0.05). Conclusions: A UIC of 500~800 μg/L is an independent TAI risk factor. The selenium intake modifies the UIC–thyroid antibody positivity relationship, with the association disappearing at high selenium levels.
Keywords:
iodine; selenium; TPOAb; TgAb; thyroid autoimmunity
Full open access here:
