Determinants of TSH change in a community-based cohort

An apparently very low-key paper - which doesn't even sound as if it is about iodine fortification, to begin with.

Dan Med J. 2016 Jan;63(1). pii: B5196.

Determinants of TSH change in a community-based cohort.

Sigurd LB1.

Author information

1 lbjergved@gmail.com; lena.bjergved.sigurd.01@regionh.dk.

Abstract

INTRODUCTION:

Thyroid disorders are common with occurrence primarily determined by the availability of dietary iodine. Iodine fortification programmes are internationally recommended to ensure sufficient iodine intake in populations. An understanding of the role of thyroid hormone levels within the normal range, set points and etiological factors related to thyroid disease development is important for optimal prevention and treatment. Limited data, however, exist regarding the impact of iodine fortification on thyroid function development. Additionally, the relation between body weight and thyrotropin (TSH) within the normal range and the role of female reproductive factors in the etiology of thyroid autoimmunity is debated.

OBJECTIVE:

The aim of this PhD project was to analyse the effect of a nationwide iodine fortification programme on individual development in thyroid function and to identify concurrent determinants for the possible changes. Furthermore, we aimed to investigate the association between weight and serum TSH change as well as the association between female reproductive factors and change in TSH and thyroid peroxidase antibody (TPO-Ab) status.

METHODS:

A longitudinal population-based study of the DanThyr C1 cohort examined before (1997-1998) and after (2008-2010) the introduction of mandatory iodine fortification of salt on July 1 2000. A total of 2,465 individuals participated in the follow-up examination. The main outcome measure was change in serum TSH. Change in TPO-Ab status was additionally used in Paper III.

RESULTS:

Urinary iodine excretion levels increased significantly during follow-up. Serum TSH also increased significantly, most pronounced in the region with the highest iodine intake, whereas the increase was not significant in the low-iodine-intake region. The presence of TPO-Ab at baseline and absence of goitre and multiple nodules were identified as determinants of TSH increase. Moreover, a low-normal TSH at baseline was a determinant of future decreased serum TSH, while likewise a high-normal baseline TSH values determined a TSH above normal reference range at follow-up. A positive association between 11-year serum TSH change and weight change was found, but without baseline body mass index being a determinant of future weight change and without baseline TSH being a determinant of future weight change. An inverse association between the time on HRT treatment and the risk of increased TPO-Ab status during follow-up was found, but the association was not significant when applying the Bonferroni adjusted significance level and not associated with TSH change. Parity, OCP use, abortions, age at menarche and menopausal status were associated neither with TSH change nor with increased TPO-Ab status during follow-up.

CONCLUSION:

TSH increased significantly, and the difference between regions with different iodine intakes could indicate that iodine, at least partly, explains the TSH increase. The identified determinants of TSH change may indicate that susceptible individuals were subject to well-known adverse effects of iodine fortification. The predictive value of TSH on future TSH levels suggests a gradual development of thyroid disease. Whether body weight and TSH are causally connected remains to be proven. These results are an important contribution to the discussion of the role of thyroid hormones level within the normal range, set points and the association with body weight. A minor role, if any, is suggested for the studied female reproductive factors in development of thyroid autoimmunity. The longitudinal study neither solves the problem of causality nor is of the optimal design to measure the impact of iodization of salt, but can be informative in the study of determinants.

PMID: 26726909 [PubMed - in process]

ncbi.nlm.nih.gov/pubmed/267...

The full paper is available here:

danmedj.dk/portal/page/port...

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9 Replies

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  • Would have been useful to know the iodine status of the individuals before the salt was introduced.. Is Denmark a high fish eating country, and so would most be iodine replete there? Do tsh levels rise in iodine deficient individuals given iodine? Or just in those over dosed with it?

  • They do eat quite a bit of fish.

    They were, as a nation, not iodine-replete.

    I agree - we want more information. Most especially as there is clearly concern about iodine here in the UK. In other times I suspect we might already have started our own iodisation process.

  • Yes, proper studies are needed to move off association and investigate cause. And I would think they need to be looking at t3 and antibodies, not just tsh.

    I've read on ne iodine site that actually iodine in salt is very unstable and not very effective as a way of raising levels. Very hard to know what is true.

    If iodine can leave the body fairly easily in urine, I wonder in what circus you would get overdose? Kidney damage?

  • Given the drive to lower people's salt intake, I wonder how many would actually ingest enough salt to make a difference.

  • Quite.

    The same issue might also apply to things like the current discussion about adding folic acid to wheat flour/bread. There is little sense in doing this if a sizeable proportion of those who should benefit don't even consume wheat products.

  • Circumstances. I hate computers.

  • Just found this in an Indian study of pregnant women in an iodine deficient area, where salt had been iodised. This was not enough to get women into a safe zone, it seems. So iodised salt may not be that effective....

    On a related topic, It is posssible that (this is my speculation) a low iodine status in undiagnosed hypothyroids could be partly responsible for the increase in risk of autism in offspring. That could help explain why the risk appears to be in undiagnosed, not diagnosed hypos - in diagnosed hypos the iodine in the levo could be helping, as well as the crucial improved activity of the thyroid itself.

    "Thirteen (28.88%) pregnant mothers had UIEs of <150 μg/L, which were below the cut-off point of the UIE for pregnant mothers. Overall, 33 mothers were from the Terai region; among them, one third had UIEs of <150 μg/L. Among the 45 pregnant women, 15 (33.34%) were not using iodised salt and the rest were using iodised salt. Among those who were using iodised salt (30 out of 45), 8 pregnant women had UIEs of <150 μg/L and among those who were not using iodised salt, 5 pregnant women had UIEs of < 150 μg/L.

    Conclusion: The UIE was below 150μg/L in a substantial percentage (28.89%) of pregnant women of the Terai region, regardless of their intake of iodised salt."

  • ironically I was diagnosed after a traumatic event, losing a lot of weight so underweight and not eating and I had changed to sea salt without iodine not realizing what I was doing for a couple years before diagnosis as well. But do eggs have iodine in them.......and 3 a day would be efficient...?

    this study is hard to understand without before and after lab test on individuals.....and if only salt was used to raise iodine and not kelp or other source...seem more info needed

  • Iodine content of eggs is variable - which makes it difficult to know how much they contain. But they don't tend to be renowned for high iodine content.

    Some time ago I posted a story about iodine-enriched eggs.

    healthunlocked.com/thyroidu...

    The reason for the study was the introduction of iodised salt - though another intervention could have been chosen (e.g iodised oil).

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