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Moreno-Reyes, Vanderpas
Nutritional epidemiology and thyroid hormone metabolism.
Vanderpas J.
Annu Rev Nutr. 2006;26:293-322. Review.
[abstract only]
"Severe iodine deficiency was the main cause of endemic goiter and cretinism. Most of the previously iodine-deficient areas are now supplemented, mainly with iodized salt. The geographical distribution of severe endemic areas has been progressively reduced, and at present, approximately 200 million people living in remote places are still at risk of severe iodine deficiency. International public health programs should be focused first on reaching these populations, and second on auditing and monitoring the operational work of supplementation programs. This second point is essential to prevent iodine-induced hyperthyroidism or interruptions of iodine supplement distribution, which could be catastrophic for the fetus and the young infant. Echography brings a complementary tool to clinical assessment of goiter by palpation. Inductively coupled plasma-mass spectrometry brings at least a definitive gold standard for iodine measurement and thyroid hormone measurement. Thiocyanate overload has been clearly documented as a goitrogen in Central Africa, and when associated with selenium deficiency, it may be included as risk factor for endemic myxedematous cretinism. Variable exposure to different environmental risk factors is likely the explanation of the variable distribution of two types of endemic cretinism (neurological and myxedematous), and the clinical overlap of the pathogeny of both syndromes is more important than previously described. It is possible that Kashin-Beck osteoarthropathy is another evanescent endemic disease that will disappear with the correction of iodine deficiency."
Selenium and iodine supplementation of rural Tibetan children affected by Kashin-Beck osteoarthropathy.
Moreno-Reyes R, Mathieu F, Boelaert M, Begaux F, Suetens C, Rivera MT, Neve J, Perlmutter N, Vanderpas J.
Am J Clin Nutr. 2003 Jul;78(1):137-44.
"BACKGROUND: Kashin-Beck disease is an osteoarthropathy endemic in selenium- and iodine-deficient areas around Lhasa, Tibet.
OBJECTIVE: We assessed the efficacy of selenium supplementation on disease progression.
DESIGN: A double-blind, randomized controlled trial of selenium supplementation was carried out in 324 children aged 5-15 y who had Kashin-Beck disease. Two hundred eighty children received iodized oil before being randomly assigned to receive selenium or placebo, and a control group of 44 subjects was not supplemented at all. Clinical and radiologic signs, selenium status, urinary iodine, and thyroid function were evaluated at baseline and at 12 mo.
RESULTS: The frequencies of joint pain, decreased joint mobility, and radiologic abnormalities were not significantly different between the 3 groups at 12 mo. Height-for-age z scores increased significantly in the subjects who received placebo and iodine or selenium and iodine. In contrast, unsupplemented control subjects did not recover from growth retardation. Serum selenium concentrations at 12 mo were within the reference range and were significantly greater in the selenium-iodine group than in the placebo-iodine group. Serum thyroid hormone concentrations were within the reference ranges after the administration of iodine, and these values were not significantly affected by selenium supplementation.
CONCLUSIONS: The results of this study do not rule out the possibility that selenium may help to prevent the occurrence of Kashin-Beck disease. However, selenium supplementation had no effect on established Kashin-Beck disease, growth, or thyroid function once iodine deficiency was corrected. These results suggest that iodine, but not selenium, deficiency should be corrected in Tibetan children with Kashin-Beck disease."
Selenium, iodine and fungal contamination in Yulin District (People's Republic of China) endemic for Kashin-Beck disease.
Zhang WH, Neve J, Xu JP, Vanderpas J, Wang ZL.
Int Orthop. 2001;25(3):188-90.
[abstract only]
"We studied the status of selenium, iodine and fungal contamination in 353 school children (age 5-14 years) from four rural villages in the District of Yulin. In three villages Kashin-Beck disease (KBD) was endemic, whereas there were no cases of KBD in the fourth village. Clinical, biological and radiological examinations (right hand) were performed and KBD was established by X-ray diagnosis. The prevalence rate of KBD was 30.2%, 44.2% and 45.3% in the three endemic villages. Mean hair selenium and urine iodine concentrations were lower in affected than in unaffected children and fungal contamination in cereal grains stored in families with KBD was more elevated than in families without KBD. Low hair selenium concentration and presence of fungal cereal contamination were significantly associated with an increased risk of KBD, but low urine iodine was not."
Epidemiological support for a multifactorial aetiology of Kashin-Beck disease in Tibet.
Suetens C, Moreno-Reyes R, Chasseur C, Mathieu F, Begaux F, Haubruge E, Durand MC, Neve J, Vanderpas J.
Int Orthop. 2001;25(3):180-7.
"We carried out a cross-sectional study in 12 rural villages in order to identify the risk factors for Kashin-Beck disease in Tibet. Children aged 5-15 years (n=575) were examined and their corresponding houses were visited. Samples were collected in order to study fungal contamination of stored grain and the organic matter content of drinking water. Multivariate analysis was performed using logistic regression and population attributable fractions were computed to estimate the impact of each factor. The following variables were independently associated with the disease: age, gender, low socio-economic status, indicators of a poorly diversified diet, iodine deficiency and small water container size (with higher organic matter levels in small containers). Selenium deficiency was severe in all study subjects. The degree of fungal contamination of barley grain was related to the highest percentage of cases (65%) in a sample of the study population. Higher urinary iodine levels were not associated with decreasing prevalence rates when Alternaria sp. was isolated. The data that we report supports the hypothesis that Kashin-Beck disease occurs as a consequence of oxidative damage to cartilage and bone cells when associated with decreased antioxidant defence. Another mechanism that may coexist is bone remodelling stimulated by thyroid hormones whose actions can be blocked by certain mycotoxins."
Kashin-Beck disease and iodine deficiency in Tibet.
Moreno-Reyes R, Suetens C, Mathieu F, Begaux F, Zhu D, Rivera T, Boelaert M, Neve J, Perlmutter N, Vanderpas J.
Int Orthop. 2001;25(3):164-6.
[abstract only]
"We evaluated iodine and selenium status in 575 children between 5 and 15 years with Kashin-Beck disease from endemic and non-endemic areas. Of these 267 (46%) children had goiter. The proportion of subjects with goiter was higher in the villages with Kashin-Beck disease than in the control village. In the villages with Kashin-Beck disease, 105 (23%) of the subjects had a serum thyrotropin greater than 10 mU/l as compared with 3 (4%) in the control village. The percentages of low serum thyroxine values and low serum tri-iodothyronine were greater in the villages where Kashin-Beck disease was endemic than in the control village. The percentages of low urinary iodine concentration were significantly greater in the subjects with Kashin-Beck disease. The results suggest that in areas where severe selenium deficiency is endemic, iodine deficiency is a risk factor for Kashin-Beck disease."
[Kashin-Beck disease in China: osteochondrodysplasia related to nutrition and environment]
Vanderpas J, Neve J.
Bull Mem Acad R Med Belg. 1999;154(3-4):177-84; discussion 184-9. French.
[abstract only]
"Kashin-Beck disease is a endemic juvenile osteochondrodysplasy, whose association with selenium deficiency and/or mycotoxin toxicity has been corroborated by epidemiological studies in China, including Tibet. Iodine deficiency appears to be a new etiological factor. Together with the geographical and epidemiological exploration of the disease, scientific multidisciplinary investigations (clinics, radiological imaging, histology, environmental and molecular biology) should afford to understand the cause of the disease before it disappears as a consequence of the evolution of the Chinese Society, including in Tibet."
Kashin-Beck osteoarthropathy in rural Tibet in relation to selenium and iodine status.
Moreno-Reyes R, Suetens C, Mathieu F, Begaux F, Zhu D, Rivera MT, Boelaert M, Neve J, Perlmutter N, Vanderpas J.
N Engl J Med. 1998 Oct 15;339(16):1112-20.
"BACKGROUND AND METHODS: Kashin-Beck disease is a degenerative osteoarticular disorder that is endemic to certain areas of Tibet, where selenium deficiency is also endemic. Because selenium is involved in thyroid hormone metabolism, we studied the relation among the serum selenium concentration, thyroid function, and Kashin-Beck disease in 575 subjects 5 to 15 years of age in 12 villages around Lhasa, Tibet, including 1 control village in which no subject had Kashin-Beck disease. Clinical, radiologic, and biochemical data were collected.
RESULTS: Among the 575 subjects, 280 (49 percent) had Kashin-Beck disease, 267 (46 percent) had goiter, and 7 (1 percent) had cretinism. Of the 557 subjects in whom urinary iodine was measured, 66 percent had a urinary iodine concentration of less than 2 microg per deciliter (157 nmol per liter; normal, 5 to 25 microg per deciliter [394 to 1968 nmol per liter]). The mean urinary iodine concentration was lower in subjects with Kashin-Beck disease than in control subjects (1.2 vs. 1.8 microg per deciliter [94 vs. 142 nmol per liter], P<0.001) and hypothyroidism was more frequent (23 percent vs. 4 percent, P=0.01). Severe selenium deficiency was documented in all villages; 38 percent of subjects had serum concentrations of less than 5 ng per milliliter (64 nmol per liter; normal, 60 to 105 ng per milliliter [762 to 1334 nmol per liter]). When age and sex were controlled for in a multivariate analysis, low urinary iodine, high serum thyrotropin, and low serum thyroxine-binding globulin values were associated with an increased risk of Kashin-Beck disease, but a low serum selenium concentration was not.
CONCLUSIONS: In areas where severe selenium deficiency is endemic, iodine deficiency is a risk factor for Kashin-Beck disease.
PIP: Selenium is involved in thyroid hormone metabolism. Kashin-Beck disease is a degenerative osteoarticular disorder endemic to certain areas of Tibet, where selenium deficiency is also endemic. Findings are reported from an investigation of the relationship among serum selenium concentration, thyroid function, and Kashin-Beck disease in 575 subjects aged 5-15 years in 12 villages around Lhasa, Tibet, including 1 control village in which no one had Kashin-Beck disease. Clinical, radiologic, and biochemical data were collected. 280 (49%) subjects had Kashin-Beck disease, 267 (46%) had goiter, and 7 (1%) had cretinism. Of the 557 subjects in whom urinary iodine was measured, 66% had a urinary iodine concentration of less than 2 mcg/dl. Mean urinary iodine concentration was lower in subjects with Kashin-Beck disease than in control subjects and hypothyroidism was more frequent. Severe selenium deficiency was documented in all villages, with 38% of subjects having serum concentrations of less than 5 ng/ml. When age and sex were controlled for in a multivariate analysis, low urinary iodine, high serum thyrotropin, and low serum thyroxine-binding globulin values were associated with an increased risk of Kashin-Beck disease, but a low serum selenium concentration was not."