That's one of the reasons it's recommended to take vit C, about 3 grams per day. Dr. Abraham wrote that vit C would improve the NIS, and since vit C is a reliable antioxidant anyway, you get coverage for both at the same time.
Evidence that the administration of Vitamin C improves a defective cellular transport mechanism for iodine: A Case Report
Guy E. Abraham, M.D. (1)and David Brownstein, M.D.(2)
Orthoiodosupplementation is the daily amount of the essential element iodine needed for whole body sufficiency (1). Whole body sufficiency for iodine is assessed by an iodine/iodide loading test (2). The test consists of ingesting 4 tablets of a solid dosage form of Lugol (Iodoral®), containing a total of 50 mg iodine/iodide. Then urinary iodide levels are measured in the following 24 hr collection. The iodine/iodide loading test is based on the concept that the normally functioning human body has a mechanism to retain ingested iodine until whole body sufficiency for iodine is achieved. During orthoiodosupplementation, a negative feedback mechanism is triggered that progressively adjusts the excretion of iodine to balance the intake. As the body iodine content increases, the percent of the iodine load retained decreases with a concomitant increase in the amount of iodide excreted in the 24 hr urine collection. When whole body sufficiency for iodine is achieved, the absorbed iodine/iodide is quantitatively excreted as iodide in the urine (1-3).
In the first study of the loading test in 6 normal subjects, the percent of loading dose of iodine excreted in the 24 hr urine collection was 39 ± 17.2 (mean ± SD) with a range of 14.2 to 66% (2). In 8 patients not receiving iodine supplementation, a mean value of 40% was reported (4). Recently, more than 4,000 loading tests were performed in the U.S. population by the Flechas Family Practice Laboratory using our procedure (2). The amount of the iodine load excreted in the 24 hr collection averages 40%, covering a wide range of ages of both sexes (5).
After 3 months of supplementation with 50 mg iodine/iodide/day, most non-obese subjects not exposed to excess goitrogens achieved whole body iodine sufficiency, arbitrarily defined as 90% or more of the iodine load excreted in the 24 hr urine collections (2-6). Adult subjects retained approximately 1.5 gm of iodine when they reach sufficiency (3). Baseline serum inorganic iodide levels 24 hrs after last dose of iodine in 8 normal subjects with normal body weight who achieved whole body iodine sufficiency had a mean ± SD of 1.1 ± 0.18 mg/L (3,7). We have arbitrarily defined as a normally functioning iodine retention mechanism, baseline serum inorganic iodide levels between 0.65 and 1.3 mg/L 24 hrs after the last dose of iodine in a subject who excretes 90% or more of the ingested iodine (7).
In patients with a normal gastrointestinal absorption of iodine but with a very defective iodine retention system, the absorbed iodine is quantitatively excreted in the urine with little or no retention. In these rare cases, the loading test will suggest whole body iodine sufficiency (90% or more excreted) but the serum inorganic iodide levels 24 hrs after the iodine load will remain low (less than 0.13 mg/L). The inefficient iodine retention mechanism could be due to either a defective cellular iodine transport system, or due to blockage of this iodine cellular transport by goitrogens that compete with iodide for the halide binding site of the symporter system. The defective iodine cellular transport mechanism could be due to genetic defects or oxidative damage to the halide binding site of the symporter (6).
We previously reported a defective cellular transport system for iodine in two obese female subjects not responding to orthoiodosupplementation (6). These individuals had low serum iodide levels (0.011 mg/L and less than 0.006 mg/L) combined with high urinary excretion of iodide following the loading test (96% and 102%). We would like to report a third case of cellular iodide transport damage in a non-obese female subject with a past history of hyperthyroidism followed by hypothyroidism treated with Synthroid 50 µg/day over the last 4 years. The other treatment modalities were added to the thyroid hormone therapy which served as baseline. The patient developed symptoms of hyperthyroidism following implementation of orthoiodosupplementation with 50 mg iodine/day. She titrated her iodine dose down to 12.5 mg every other day (6.25 mg average daily dose). She tolerated a daily average dose of 6.25 mg iodine well with increased energy. The iodine transport damage was corrected as least partially by administration of the antioxidant Vitamin C in a sustained released form at 3 gm/day for three months.