The Claim

Individuals with chronic fatigue syndrome who possess autoantibodies to selenoprotein P have significantly lower urinary iodine excretion compared to individuals with chronic fatigue syndrome without these autoantibodies and to healthy controls, which reflects reduced liberation of iodide from thyroid hormone due to impaired deiodinase activity.

Source: Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone

What the research says

Supports is higher

Support is ahead, but a single strong opposing study can change this.

Supports
54score
Challenges
0score

These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.

How it works
1 study reviewed
In plain English

People with chronic fatigue syndrome who have specific antibodies targeting selenoprotein P excrete less iodine in their urine than those without these antibodies or healthy individuals, suggesting a reduction in the release of iodide from thyroid hormones caused by decreased deiodinase enzyme function.

See the scientific wording

Individuals with chronic fatigue syndrome who have autoantibodies to selenoprotein P exhibit significantly lower urinary iodine excretion than those without these autoantibodies or healthy controls, indicating reduced liberation of iodide from thyroid hormone due to impaired deiodinase activity.

What the research says

1 study
  1. Study: Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone

    People with chronic fatigue syndrome who have certain antibodies that block selenium transport also have much less iodine in their urine, because their bodies can't properly convert thyroid hormone into its active form — so less iodine gets released and flushed out.

Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies

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