...of lack of Iodine in the diet. Severe maternal Iodine deficiency results in cretinism of the offspring. The images presented here are of very severe cases, but I wonder what chronic deficiency, over generations, does. Add to that the fact that chlorine, fluoride, bromide are sitting on the receptors where Iodine should be...is there such a thing as subclinical cretinism? I think yes...read it and weep, folks, in the link below, "Iodine deficiency results in a global loss of 10-15 IQ points at a population level and constitutes the world's greatest single cause of preventable brain damage and mental retardation."

~Anyone got any stats on the declining IQs of the US' children?



http://pmj.bmj.com/cgi/content/abstract/77/906/217


Iodine deficiency as a cause of brain damage

"This editorial reviews the impact of iodine deficiency (1) on thyroid function in pregnant women and neonates and (2) on the neurointellectual development of infants and children.

All degrees of iodine deficiency (mild: iodine intake of 50-99 µg/day, moderate: 20-49 µg/day, and severe: <20 µg/day) affect thyroid function of the mother and the neonate as well as the mental development of the child. The damage increases with the degree of the deficiency, with overt endemic cretinism as the severest consequence.

Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism in cretins.

Iodine deficiency results in a global loss of 10-15 IQ points at a population level and constitutes the world's greatest single cause of preventable brain damage and mental retardation."






http://en.wikipedia.org/wiki/Cretinism


"Endemic cretinism arises from a diet deficient in iodine and has affected far more people worldwide and continues to be a major public health problem in many countries. Iodine is an essential trace element, necessary primarily for the synthesis of thyroid hormones. Although it is found in many foods it is not universally present in all soils in adequate amounts. The soils of many inland areas on all continents are iodine deficient, and plants and animals grown there are correspondingly deficient. Populations living in those areas without outside food sources are most at risk for iodine deficiency diseases.
Iodine deficiency results in the impairments of varying degrees of physical and mental development. It also causes gradual enlargement of the thyroid gland, referred to as a Goitre. It is being combatted in many countries by public health campaigns of iodine administration."

~I wonder why this is no longer addressed in the good old USA???????






http://www.unu.edu/unupress/food/8f044e/8F044E03.htm


China is battling cretinism in inland areas with iodized salt...

CLINICAL MANIFESTATIONS OF ENDEMIC CRETINISM

"The clinical picture of endemic cretinism in China is quite variable. The common type is neurological cretinism, but typical myxoedematous cretinism can also be seen in some endemias of this country. A number of mixed forms characterized by either predominant neurological defects or predominant hypothyroidism have been found in other parts of the country. The classification of the two types of cretins is based on the following criteria:
i.Mental retardation is the common criterion in both types.
ii.Neurological cretins have predominantly neurological manifestations, such as abnormalities in hearing and speech, congenital diplegia, strabismus, and only occasionally myxoedema.
iii.Myxoedematous cretins have predominantly hypothyroid manifestations, such as stunted growth, sexual underdevelopment, myxoedema, and other clinical symptoms and signs of hypothyroidism, and only occasionally upper motor neuron defects.
The endemic cretinism in the suburb of Chengde City, Hebei Province, was of the neurological type. During the first survey in 1961 (27, 28) the morbidity rate was 2.4 per cent; the youngest patient was 5 years of age, and the oldest was 55. Most were under 12. They all showed mental retardation, and some were profoundly retarded. Hearing and speech defects were also striking; 26.2 per cent were completely deaf, and 46.3 per cent were completely mute. Upper motor neuron defects were also quite common; 76.2 per cent had an abnormal gait, 8.6 per cent scissor gait, 27.5 per cent an exaggerated knee jerk, and 3.8 per cent had severe spastic paralysis. Pneumoencephalographic examination of four cases of cretinism showed two with widening of the subarachnoid space, indicating atrophic changes in the brain. EEG examination showed low frequency and irregular rhythm; 53.9 per cent had no alpha waves, while 92.3 per cent had paroxysmal bilateral synchronic theta waves.
Physically they showed definite developmental retardation. Their heights were 3.1 to 13.0 cm lower than normal. The ratio of the upper and lower body measurements was greater than 1. Roentgenological examination of the wrists showed delayed bone age in 76.5 per cent, but 32.7 per cent of the normal children of the same age in the same locality showed slightly delayed bone age, considered to be the result of malnutrition.
Sexual development was usually delayed in both male and female cretins. Menarche usually delayed by one to five years, yet some of these women eventually attained full maturation and gave birth normally. Only two cretins had definite myxoedema, with no other obvious signs of hypothyroidism and no enlargement of the sella turcica on radiological examination."






http://www.thyroidmanager.org/Chapter20/ch01s03.html


"Developmental neuropathology and available epidemiologic data suggest that the period from about 12-14 weeks until 20-30 weeks of gestation may be the critical period during which damage occurs (10). Cortical and striatal neuron proliferation, migration, and early formation of neuropil occur between 12 and 18 weeks. Cochlear development occurs at the same time. These data correlate well with the data from the Papua New Guinea trial which indicated that iodine repletion must occur by three months of pregnancy to prevent cretinism (35).
Studies already cited above on the effect of iodine deficiency on brain cell development in the newborn rat, sheep and marmoset suggest that iodine deficiency has an early effect on neuroblast multiplication. Brain weight is reduced with a reduced number of cells as indicated by lowered DNA, a greater density of cells in the cerebral cortex and reduced cell acquisition in the cerebellum. In the light of the recent evidence summarized above (Iodine deficiency in the foetus) that maternal thyroxine crosses the placenta, it is now envisaged that neurological cretinism is predominantly caused by maternal hypothyroidism due to iodine deficiency. It has been suggested that an autosomal recessive predisposition, besides maternal iodine deficiency, may play an etiological role in neurological cretinism."


http://www.jci.org/cgi/content/full/99/11/2701


"Alterations of thyroid function during human development are known to produce extensive damage to the central nervous system (CNS)1 (for reviews see references 1), including severe mental retardation. The most severe alterations are not those encountered in untreated congenital hypothyroidism, but in the neurological cretins born in areas of marked nutritional iodine deficiency (5). When newborns with congenital hypothyroidism are treated with L-thyroxine (T4) soon after birth, severe mental retardation is avoided (9). On the contrary, in the case of iodine deficiency, the major CNS damage is already irreversible by birth and can only be prevented by correction of the maternal iodine deficiency early in pregnancy (10, 11). Neurological abnormalities (6, 12, 13) include hearing and speech defects (often resulting in deaf-mutism), mental deficiency (intellectual deficits, visuomotor integration deficits, release of primitive reflexes, autism, and vacuity), and motor deficits (proximal and truncal rigidity, flexion distonia, spasticity, muscle wasting, and thalamic posturing). It has been concluded from the clinical findings (7) that the underlying anatomic lesions are likely to implicate the cochlea, cerebral cortex, association cortex, frontal lobe, amygdala, hippocampus, right hemisphere cortex, basal ganglia (putamen and globus pallidus), corticospinal tracts (including the premotor cortex), lower motor neurons, and severe cortico-striatal motor lesions. The clinical presentation covers a wide spectrum of different combinations of the above findings. Except for the mental retardation, these abnormalities are rarely found in congenital hypothyroidism, even when left untreated after birth."

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and it has been suggested that Neanderthals were *gasp* iodine deficient...a.k.a CRETINS. In which direction is the human race evolving today?






http://www.trussel.com/prehist/news125.htm


"In a controversial paper published in the Geographical Review, Jerome Dobson, a geographer at Tennessee's Oak Ridge National Laboratory, has suggested that the Neanderthals could have been a kind of modern human who suffered from chronic iodine deficiency and cretinism that caused the thick, curved bones, large heads, ridged eyebrows and heavy muscles that are typical Neanderthal characteristics.
Dobson noted that the map of sites where Neanderthal remains have been found corresponds fairly closely to a pattern of cretinism common in the "goiter belts" of Central and Alpine Europe until well into the 20th century, when iodized salt was introduced.
"Neanderthalism" may have ended only when modern humans figured out how to bring iodine inland, he said. Seaweed, marine fish and shellfish are nature's prime sources of iodine."