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Cretinism

Cretinism (most likely from the Latin Christiānum, "Christian") is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones (hypothyroidism). The term cretin refers to a person so affected. more...

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Etymolology and usage of the term

The term cretin was brought into medical use in the 18th century from an Alpine French dialect where persons with such a condition were especially common (though the cause was unknown). It was used widely as a medical term in the 19th and early 20th centuries, but in recent decades has spread more widely in popular English as a markedly derogatory term for a hopelessly stupid person. Because of its pejorative connotations in popular speech, the term has been largely abandoned by physicians. A cretin of the Pyrenees was called a cagot (kag'ō).

The etymology of the word cretin is not known with certainty. Several hypotheses have been proposed. The most common derivation provided in English dictionaries is from the Latin Christiānum (Christian), via a medieval French dialect (compare modern French chretien). The connecting meaning between "Christian" and "cretin" is not obvious. According to the Oxford English Dictionary, the translation of the Latin term into "human creature" implies that the label "Christian" is a reminder of the humanity of the afflicted, in contrast to brute beasts . Other sources have suggested "Christian" refers to the inability to sin of such a person who lacks the capacity to distinguish right from wrong .

Other speculative etymologies have been offered:

  1. From creta, Latin for chalk, because of the pallor of those affected.
  2. From cretira, Grisson-Romance creature, from Latin creatus.
  3. From cretine, French for alluvium (soil deposited by flowing water), an allusion to the suspected origin from inadequate soil.
    Source: VC Medvei. The History of Clinical Endocrinology. Pearl River, New York: Parthenon Publishing Group. 1993.

Cretinism due to congenital hypothyroidism

Congenital hypothyroidism can be endemic, genetic, or sporadic. If untreated, it results in mild to severe impairment of both physical and mental growth and development.

Poor length growth is apparent as early as the first year of life. Adult stature without treatment ranges from 1 to 1.6 meters, depending on severity, sex and other genetic factors. Bone maturation and puberty are severely delayed. Ovulation is impeded and infertility common.

Neurological impairment may be mild, with reduced muscle tone and coordination, or so severe that the person cannot stand or walk. Cognitive impairment may also range from mild to so severe that the person is nonverbal and dependent on others for basic care. Thought and reflexes are slower.

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Prevention of cretinism by iodine supplementation during pregnancy - adapted from the New England Journal of Medicine, December 29, 1994
From Nutrition Research Newsletter, 2/1/95

Endemic cretinism, caused by severe iodine deficiency during pregnancy, is a major cause of mental retardation in some parts of the world. Despite iodine supplementation programs, endemic cretinism is still found in southern and eastern Europe and is common in Asia, Africa, and Latin America; the prevalence may be as high as 10% in some communities. In 1990, the World Health Organization estimated that 20 million people in the world had preventable brain damage due to the effects of iodine deficiency on fetal brain development.

Endemic cretinism can be prevented by iodine supplementation before conception. Previous studies have not established, however, whether supplementation during pregnancy or in early childhood would be of value in reducing the risk.

In a new study conducted in a severely iodine-deficient area of the Xinjiang region of China, iodine was administered to women in various stages of pregnancy and to children from birth to age three years. The treated children and offspring of treated women were followed for two years. Three independent measures of neural development were assessed.

Iodine supplementation during the second trimester of pregnancy was clearly beneficial in reducing the prevalence of moderate and severe neurologic abnormalities. Iodine supplementation during the first trimester may have been effective as well, but difficulties in administering the required dose to this group of women prevented definitive conclusions from being reached. Iodine administration during the third trimester or after birth was less valuable; it did not improve neurologic status, but head growth and developmental quotients improved slightly.

These findings indicate that supplementation with iodine before the end of the second trimester of pregnancy can protect the fetal brain from the effects of iodine deficiency. "It is obviously preferable to start providing iodine before pregnancy and to provide it continuously." However, supplementation during early pregnancy would be of value in instances where adequate iodine intake cannot be ensured before conception.

Cao Xue-Yi, Jiang Xin-Min, Dou Zhi-Hong et al, Timing of Vulnerability of the Brain to Iodine Deficiency in Endemic Cretinism, New England J Medicine 331(26):1739-1744 (29 Dec 1994) [Reprints: G Robert DeLong, MD, Division of Pediatric Neurology, Duke University Medical Center, Box 3936, Durham NC 277101

Basil S Hetzel, Iodine Deficiency and Fetal Brain Damage [Editorial], New England J Medicine 331(26):1770-1771 (29 Dec 1994) [Correspondence: Basil S Hetzel, MD, International Council for Control of Iodine Deficiency Disorders, North Adelaide, SA 5006, Australia]

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