Symptoms of Low Selenium: Causes, Diagnosis, and Treatment

Keshan disease is an endemic dilated cardiomyopathy first identified in Keshan County, Heilongjiang Province, China, in the 1930s. It primarily affects children and women of childbearing age living in a broad selenium-depleted belt stretching from northeast to southwest China. The disease causes focal myocardial necrosis — patches of heart muscle die and are replaced by fibrous scar tissue — leading to heart failure, arrhythmias, and cardiogenic shock. Before selenium supplementation programs began in the 1970s, mortality was high. The discovery that selenium deficiency caused Keshan disease was a landmark in nutritional science: researchers mapped soil selenium levels across China and found a near-perfect geographic correlation between low soil selenium and disease incidence.

Kashin-Beck disease is an endemic osteoarthropathy affecting children and adolescents in selenium-poor, iodine-poor mountainous regions of China, Tibet, and Eastern Siberia. It causes cartilage necrosis, joint deformity, and growth retardation — children develop stiff, painful, enlarged joints that can lead to permanent disability. The etiology is complex: selenium deficiency is a necessary factor, but researchers believe additional triggers — possibly mycotoxins from Fusarium fungi on stored grain, or organic compounds in drinking water — contribute to the full disease expression. Unlike Keshan disease, Kashin-Beck has proven harder to eliminate through selenium supplementation alone, suggesting a multifactorial cause.

The common thread is geography. Unlike most minerals, there is no homeostatic regulation of selenium uptake from soil into plants — crops simply reflect the selenium content of the soil they grow in. This means food selenium varies enormously by agricultural region. Wheat grown in the selenium-rich soils of the US Great Plains can be a meaningful dietary source; wheat from selenium-depleted regions of China or parts of Europe contributes almost nothing. Your location — specifically, where your staple grains were grown — is a major determinant of selenium intake in ways that don't apply to most other nutrients.

The problem is that Brazil nut trees (Bertholletia excelsa) are hyperaccumulators of selenium — they concentrate it from soil far more aggressively than other plants. If the soil is selenium-rich (as in parts of the Amazon basin), the nuts contain enormous amounts. If the soil is poor, they contain modest amounts. You cannot tell by looking at the nut. Eating one to two Brazil nuts daily is probably safe for most people and will meet the RDA, but eating four to six daily — especially alongside a selenium-containing multivitamin or a diet rich in seafood — can push total intake above the 400 mcg UL. For people who want a predictable selenium source, Brazil nuts are not it.

Reliable, moderate selenium sources are abundant in a standard omnivorous diet. Cooked yellowfin tuna provides approximately 92 mcg per 3-ounce serving. Halibut delivers roughly 47 mcg. Sardines, shrimp, and cod are also good sources. Among meats, lean beef, turkey, and chicken contribute meaningful amounts. Eggs contain about 15 mcg each. The key point is that a varied diet including seafood a few times per week and regular meat or egg consumption easily meets the 55 mcg RDA for most North Americans — without supplementation.

Grain selenium content is highly region-dependent. Wheat grown in the selenium-adequate soils of the US Great Plains contributes to dietary intake; wheat from selenium-poor European or Chinese soils contributes little. Cooking methods matter modestly — boiling can leach some selenium into cooking water, but heat does not destroy selenium the way it degrades certain vitamins. For supplementation, selenomethionine (the organic form found in foods) has higher bioavailability than inorganic sodium selenite and is the form used in most clinical trials, including the Hashimoto's studies.