Author: Chiara Campagnaro
Date: 10/12/2009


Kombu or Laminaria Japonica is large seaweed, which belongs to the brown algae and it is classified in the order of Laminariales. Kombu is an important food source in many Asian cultures, while in occidental it is principally used by vegetarians.

Kombu contains:

  • iodine 8000 mg/100g
    • potassium 6100 mg
    • calcium 710 mg
    • iron 3.9 mg
    • carotene 1100 μg
    • vitaminB1 0.48 mg
    • vitaminB2 0.37 mg
    • dietary fiber 27.1g
    • energy 145kcal (per 100gr)
    • glutamic acid

In medicine Kombu is required:

  • to promote the thyroid gland hormone;

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• to prevent a rise of blood pressure, cholesterol and blood sugar level;
• to cure intestinal disorders

As Iodine supply in dietary Iodine deficiency

Since Kombu contains a high iodine contents, it has an effect for thyroid gland. Indeed, iodine is an essential element of thyroid hormones. Thus changes in iodine intake can cause various thyroid disorders. Thyroid hormones, 3,5,3-triiodothyronine (T3) and thyroxine (T4), are implicated in the regulation of metabolism, growth and maturation of a variety of organ systems. The daily requirement of iodine is :
ADULT : 150µg/die
PREGNANT : 250µg/die
<2 years 90µg/die

Effects of excessive Iodine intake


In literature, it is proved that Kombu is used by an increasing number of patient and people. According to the prevailing belief that herbal products are safe owing to their natural origin, most of people use Kombu as dietary supplements. However, many serious and side effects have been recently reported. Kombu has different side effected as toxicity and allergic reactions, moreover Kombu can interact with drugs and other herbs leading to a healthy problems.
For example, an excess iodine may induce not only hyperthyroidism but also hypothyroidism, particularly in subjects living in iodine-sufficient area, neonatal or older persons, patients with underlying thyroid disorders such as autoimmune thyroid disease, subacute thyroiditis, thyroidectomy and other.
The occurrence of these 2 disparate responses to iodide excess may be due to differences in the sensitivity to iodide-induced turn-off in hormone biosynthesis. Subjects with an elevated sensitivity, such as patients previously treated for Graves' disease with radioactive iodine, subtotal thyroidectomy, antithyroid drugs, or those with chronic autoimmune thyroiditis, have an increased risk to develop hypothyroidism after administration of excessive iodide because of a failure to escape from the acute Wolff–Chaikoff effect . In contrast, in subjects with lowered sensitivity, patients with endemic goiter and iodide deficiency or patients with nodular goiter containing autonomous nodules, iodide excess may result in hyperthyroidism.
The Wolff-Chaikoff is an autoregulatory phenomenon, which inhibits formation of thyroid hormones inside of the thyroid follicle, because there is a decrease in sodium/iodide symporter (NIS) and thyroid peroxidase (TPO) due to elevated levels of circulating iodide. NIS and TPO are two proteins, that are involved in synthesis of T4 and T3. In details, NIS transports iodide (I-) across the basolateral membrane into thyroid epithelial cells. TPO is a glycosil protein. Starting from tyreoglobulin, TPO synthetizes T3 and T4 hormones. The expression of NIS and TPO genes is stimulated by thyrotropin (TSH). Wolff-Chaikoff's effect persists in several days (around 10 days), then it is followed by an "escape phenomenon", which is characterized by resumption of normal organification of iodine and normal thyroid peroxidase function. This escape phenomenon in some people could fail and leads to HYPOTHYROIDISM due to excess of iodine. Some researches [1] suggest that NIS and TPO decrease thanks to a transcriptional mechanism. Indeed, these studies report a decrease of NIS and TPO mRNA in Wolff-Chaikoff.

In [2] the authors explain the suppression of thyroid function during ingestion of seaweed “Kombu” in normal Japanese adults. Indeed, most Japanese people eats iodine-rich foods such as seaweed .
They demonstrate that the daily ingestion of Kombu over the short term (7-10 days) results in a significant increase in serum TSH with a slight decrease in serum free thyroxine (FT4) and/or free 3,5,3-triiodothyronine (FT3) concentrations. During ingestion of Kombu for long term (55-87 days) serum TSH levels are elevated, but FT3 and FT4 concentrations are almost within normal values. FT3 and FT4 concentrations are influenced by various factors such as the degrees of inhibitory effect of iodine on thyroid function, increase of TSH by the negative feedback mechanism, responsiveness and compensatory enlargement of thyroid gland to TSH.
The inhibitory action of excess iodine (acute Wolff-Chaikoff effect) is known to be temporary but in this study it is persisted in the patients for three months. This highlights that thyroid function in normal Japanese adults is suppressed during the ingestion of Kombu, although the suppression is slight and reversible.
Recently, some studies have reported that one third of cases of consecutive Hypothyroidism in Japan become euthyroid after iodine restriction.
Another study [3] proves that, although iodine supplementation should be implemented to prevent and treat iodine-deficiency disorders, supplementation should be maintained at a safe level. In fact the authors observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake. They examined the effect of regional differences in iodine intake on the incidence of thyroid disease.
Levels that are more than adequate or excessive do not appear to be safe, especially for susceptible populations with either potential autoimmune thyroid disease or iodine deficiency. Supplementation programs should be tailored to the particular region. No iodine supplementation should be provided for regions in which iodine intake is sufficient, whereas in regions in which iodine intake is deficient should be supplemented with iodine according to the degree of iodine deficiency.
But in the most cases the not-controlled assumption of Kombu leads to HYPERTHYROIDISM.
A 39-year-old woman (157 cm, 75 kg, body mass index [BMI] 30.4 kg/m2) with enlarged thyroid.
The patient’s medical history and family history were unremarkable.
Medical examination confirmed a palpably enlarged thyroid.
Normal values of FT3, FT4, and TSH were congruent with the lack of clinical signs of hyper- or hypothyroidism; anti-TPO, antithyroglobuline (TG), and anti-TSH-receptor (TSH-R) antibodies were negative.


fT4 (ng/dL) fT3 (pg/dL) TSH (mU/L) TPO-AB (kU/L) TG-AB (kU/L) TSH-R-AB (U/L)
0.8–1.7 210–420 0.4–2.5 <1.9 <0.9 <12

Ultrasonography revealed a multinodular goiter with a total volume of 62 mL. A thyroid 99mTC-pertechnetate scintigraphy showed a homogenous uptake with a moderate autonomy in the right upper lobe, confirmed by a thyroid scan under exogenous TSH suppression with levothyroxine.

The patient was informed of the therapeutic options: 1)thyroid resection; 2) routine follow-up clinical visits. She decided against surgery, so that a short-term control visit was arranged. Furthermore, it was pointed out to the patient to avoid the intake of large amounts of iodine, such as iodinated radiocontrast agents or iodine-containing drugs or food. Two months later, the patient was in good general health and endocrine tests revealed thyroid hormones and TSH plasma levels within the normal range.

Four months after the initial visit, the patient showed typical signs of hyperthyroidism, including tachycardia (100 beats/min), palpitations, tremor, nervousness, insomnia, fatigue, increased sweating, diarrhea, secondary amenorrhoea, and weight loss. The laboratory analysis revealed increased levels of FT3 and FT4 as well as a suppressed TSH concentration and anti-thyroid antibodies remained negative. Ultrasonography showed a multinodular goiter with a total volume of 67 mL. The patient did not report any exposure to medications containing iodine, such as iodinated radiocontrast agents or amiodarone. However, on further questioning, the patient reported that for the last 4 weeks she had been consuming a herbal tea, prescribed by a Chinese alternative practitioner to treat her enlarged thyroid. Treatment included kelp, Sargassum weed, and Kombu.
Then, the patient was advised to discontinue the consumption of the tea and an antithyroid drug therapy was initiated. Her follow-up visit, 7 months after the diagnosis of hyperthyroidism, revealed normal laboratory values.

In another case [5], an excess of iodine can obstruct the therapy:
A 55-year-old man had a large mass on the right side of his neck, which was identified in a specimen from a fine-needle aspiration biopsy as papillary thyroid carcinoma . He had a total thyroidectomy and the pathological examination revealed a multifocal, papillary thyroid carcinoma with metastases in 26 of 78 lymph nodes. Ablation with radioiodine was recommended, but the patient had undergone computed tomographic (CT) scanning with an iodine-rich contrast agent 2 months earlier. The level of urinary iodine was elevated and remained elevated after 10 days on furosemide, a diuretic. The patient reported having ingested a large number of supplements, included selenium. The selenium supplement was the source of the excess iodine, which is found in kelp, an inactive ingredient in the supplement.
He did not resume taking the supplements and was again placed on a low-iodine diet for 4 weeks and the level of urinary iodine was decreased.
Physician who use radioiodine are aware that excess exogenous iodine impairs the efficacy of iodine-131 therapy. In this patient, excessive iodine intake came from an unexpected source (kelp-enriched selenium). The iodine content of kelp is highly variable, and it is likely that the iodine levels in different batches of kelp-enriched selenium are also highly variable. Although it is not routine to assess urinary iodine concentrations in patients receiving radioiodine, it needs for physicians to review patients’ medications and dietary habits carefully to prevent ingestion hidden sources of iodine.

Other researches [6] reported the consequences in neonates born to mothers with excessive iodine intake.
These neonates were exposed to elevated quantities of iodine, because their mothers consumed an excessive quantity of Kombu during the pregnancies. This exposure led to transient hypothyroidism.
Some of these newborns have required LEVO-thyroxine treatment, because hyperthyrotropinemia was persisted.


These researches show that the consumptions of seaweed as Kombu, which are promoted as healthy foods, have to be controlled and have not to exceed the daily limit needed to the person. Particularly patients, which have thyroid disorders, must inform the physician before assuming Kombu.
Since most Asian people eat a great deal of Kombu, it is necessary to warn these people against consuming excessive amounts of seaweed.
For instance, in Japan the Ministry of Health, Labour and Welfare recommended an upper intake bound of iodine as 3mg. per day [7].


1. Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein.1999

2.“Suppression of thyroid function during ingestion of seaweed Kombu (Laminaria japonica) in normal Japanese adults.” Endocrinology Journal (2008); 55 (6): 1103-1108

3.“Effect of iodine intake on thyroid disease in China” The New England Journal of Medicine (2006); 354: 2783-93

4. “Iodine induced thyrotoxicosis after ingestion of kelp containing tea”
Journal General of Internal Medicine (2006 June); 21(6): C11-C14

5. “Excess iodine from an unexpected source” The New England Journal of Medicine (2009 January); 360: 4

6. “Transient hypothyroidism or persistent hyperthyrotropinemia in neonates born to mothers with excessive iodine intake” Thyroid (2004 December); 14(12): 1077-83

7. The Ministry of Health, Labour, and Welfare, Japan (2005) “Dietary reference intakes for Japanese” (2005) In the Ministry of Health, Labour, and Welfare (ed) Daiichi Shuppan Publishing, Tokyo: 189-193


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