Pamela A. Popper, Ph.D., N.D.

Wellness Forum Health

 While cruciferous vegetables are thought by most people to be nutritious foods that contain anti-cancer properties, some health professionals caution against consuming them because of the supposed link between cruciferous vegetables and hypothyroidism.

I’m often asked by hypothyroid patients if they should lower their intake of or stop consuming cruciferous vegetables. Fortunately, the answer is “no.” There is no reliable evidence suggesting that consuming even large amounts of cruciferous vegetables results in increased risk of hypothyroidism.

The Linus Pauling Institute features an article on cruciferous vegetables, both promoting their value in lowering the risk of cancer, but also suggesting that “Very high intakes” of cruciferous vegetables “…have been found to cause hypothyroidism in animals.”[1]  The article cites a study showing that very high intake of cruciferous vegetables has been shown to induce hypothyroidism in animals.[2] But animal studies are not always reliable indicators of results in humans.

The Pauling site also includes one case report of an elderly woman who developed hypothyroidism after eating between 2.2 and 3.3 pounds of raw bok choy per day for several months.[3]  This is only a case report, and no conclusions can be drawn from case reports. There are two other issues concerning this case report. The first is that I find it highly unlikely that many people would consume such a high amount of bok choy daily for such an extended period of time, which makes this case somewhat irrelevant. The other is that I am not convinced that this woman’s hypothyroidism was caused by eating bok choy. She was elderly, had suffered a stroke, and had started eating bok choy because she believed it could help her to control her diabetes. The subject was a an elderly, very sick person who might have developed hypothyroidism without ever consuming a cruciferous vegetable. The case report refers to a study often cited in support of the cruciferous vegetable/hypothyroidism theory that was done in the 1920’s showing that rabbits eating a diet comprised almost solely of cabbage developed goiters. Rabbits are not humans, rabbits in the wild do not live exclusively on cabbage, and humans do not eat a diet of almost all cabbage either, which makes this study somewhat irrelevant too.

The Pauling site mitigates its concerns about the issue by stating that in the absence of iodine deficiency, cruciferous vegetable intake does not increase the risk of hypothyroidism.

According to Chris Masterjohn at the Weston Price Foundation, not only is there a “Dark Side of Soy,” but also a “Dark Side of Crucifers.” He states that when raw cruciferous vegetables are chewed or digested by intestinal bacteria, that goitrogens are released. He says that when intake of cruciferous vegetables is low, these goitrogens increase the need for iodine, but when intake is high, they can damage the thyroid gland. He suggests boiling cruciferous vegetables for 30 minutes in order to inactivate the goitrogens.[4]

 Masterjohn writes at length about this issue as if the connection is proven and the risk is real. A close look at his citations, however, should put most people’s minds to rest. Masterjohn cites a study in which rats were fed a diet with 30.0% of calories from radishes.  Even when the radishes were cooked and the rats were given large doses of iodine, the weight of their thyroid glands increased, and the rats showed changes in thyroid hormone levels consistent with hypothyroidism.[5] Aside from the obvious, rats are not the same as humans, radishes contain only one calorie each. This means that a person eating a 2,000 calorie-per-day diet would have to consume 600 radishes per day in order to eat 30.0% of calories from radishes. I think most people would agree that this dietary pattern would be impossible to sustain for even one day.

Masterjohn states that cruciferous vegetables also contain nitriles that “…can release cyanide into tissues and result in general toxicity at high doses.”  He then cites a study showing that doses of nitriles “that are impossible to obtain from food would be required to result in toxicity.”  Since the topic is how eating cruciferous vegetables can result in hypothyroidism, I fail to see the relevance.

Masterjohn’s article becomes even more nonsensical when he discusses the dangers of Brussels sprouts, citing another rat study in which rats were given dried Brussel’s sprouts in varying amounts and under varying circumstances. While the researchers discussed the negative effects potentially correlated with feeding Brussel’s sprouts to rats, they concluded that “…the thyroid characteristics were less sensitive to Brussel’s sprouts than were other criteria examined.”[6]

Masterjohn’s article provides more entertainment than constructive guidance, so let’s look at the issue from a more analytical standpoint. The vast majority of “evidence” showing that there is reason to be concerned about the effect of eating cruciferous vegetables on thyroid function has been conducted on animals and is based on the idea that certain goitrogens in these foods interfere with thyroid function. This is a hypothesis only, and even this hypothesis has caveats, which include that the only way cruciferous vegetables can negatively affect thyroid function is if a person suffers from iodine deficiency.

The only human intervention study I could find looking at this issue involved subjects eating 150 grams of cooked Brussel’s sprouts daily for 4 weeks and there was no effect on thyroid function.[7] Another study looked at vegetarians and vegans in Boston and showed that vegans had lower iodine intake and higher urinary levels of thiocyanate, a marker for cruciferous vegetable intake, but thyroid function was normal nonetheless.[8]

As for iodine deficiency, concerns about this issue seem to have been exaggerated. The thyroid uses about 150 mcg per day of iodine, which is easily obtained from food. A medium baked potato contains 60 mcg, 4 ounces of cranberries contains 400 mcg, and one half cup of navy beans contains 32 mcg. The National Institutes of Health says that average iodine intake in the U.S. ranges from 138 to 353 mcg per day across all age and gender groups, and this estimate does not include iodized salt.[9] There may be more reasons to be concerned about excessive iodine intake than iodine deficiency. Higher iodine intake has been linked to both hypothyroidism and autoimmune thyroiditis.[10]

The caution about eating cruciferous vegetables is an example of irresponsible fear mongering based on mostly irrelevant animal studies and unproven hypotheses.  Most studies show that these foods are health-promoting and reduce the risk of many diseases, including cancer.[11]

[1] http://lpi.oregonstate.edu/mic/food-beverages/cruciferous-vegetables

[2] Fenwick G, Heaney R, Mullin W. “Glucosinolates and their breakdown products in food and food plants.”  Crit Rev Food Sci Nutr. 1983;18(2):123-201

[3] Chu M, Seltzer T. “Myxedema coma induced by ingestion of raw bok choy.” NEJM. 2010;362(20):1945-1946.

[4] “Bearers of the Cross: Crucifers in the Context of Traditional Diets and Modern Science”

[5] Chandra AK, Mukhopadhyay S, Ghosh D, Tripathy S. “Effect of radish (Raphanus sativus Linn.) on thyroid status under conditions of varying iodine intake in rats.” Indian J Exp Biol. 2006;44:653-661.

[6] De Groot A, Willems M, de Vos R. “Effects of high levels of brussels sprouts in the diet of rats.” Food Chem Toxicol. 1991;29(12):829-37.

[7] McMillan M, Spinks E, Fenwick G. “Preliminary observations on the effect of dietary brussels sprouts on thyroid function.” Hum Toxicol 1986;5:15-19.

[8] Leung A, Lamar A, He X, et al. “Iodine status and thyroid function of Boston-area vegetarians and vegans.” J Clin Endocrinol Metab 2011;96:E1303-1307.

[9] http://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/

[10] Teng W, Shan Z, Teng X et al. “Effect of iodine intake on thyroid diseases in China.”  NEJM 2006 June 29;354(26):2783-93

[11] Higdon J, Delage B, Williams D, Dashwood R. “Cruciferous Vegetables and Human Cancer Risk: Epidemiologic Evidence and Mechanistic Basis.” Pharmacol Res 2007 Mar;55(3):224-236