This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Thyroid hormone plays a supportive role in the musculoskeletal, cardiovascular, hepatic, renal, and central and peripheral nervous systems. As a result, overt thyroid failure can induce bradycardia, decrease in body temperature, carpal tunnel syndrome from soft tissue deposition, muscle cramps, hyponatremia, anemia, impaired intestinal motility, confusion, depression, fatigue, and weakness. Thyroid hormone levels are maintained within the normal range through a classical endocrine feedback loop involving the pituitary/hypothalamus and the thyroid. A decrease in serum thyroid hormone levels is sensed by the pituitary, which in turn increases TSH production. The thyroid responds to increased serum levels of TSH by stimulating thyroid hormone secretion until the euthyroid state is once again established, at which point TSH production returns to basal levels. There are several, often unappreciated facts about this feedback mechanism. First, TSH is logarithmically related to free T4 levels, and relatively small reductions in free T4 can dramatically change the serum TSH. Second, normal levels of TSH and free T4 are typically calculated as those values within two standard deviations from the mean of normally distributed free T4 levels. In fact, however, each individual has a much tighter range of hormonal levels clustered within the overall population norm. Therefore, in the early stages of hypothyroidism, free T4 levels may move out of an individuals normal range but remain within the population norms. In overt hypothyroidism, the thyroid is damaged to an extent that serum levels of thyroid hormone drop below normal, and TSH levels continue to increase. Subclinical hypothyroidism is a common disorder, particularly in the elderly. In one large study of elderly patients in a primary care geriatric clinic, 4% of men and 15% of women had subclinical hypothyroidism (TSH 5 to 15 mU/L). The Whickham study, performed in a small town in England, showed that 17% of older individuals in the community had subclinical hypothyroidism. In the United States, 14% of patients in a senior citizen center had TSH levels between 5 and 15 mU/L. Results vary widely depending on the patient population and country. In western Germany only 4% of elderly patients were found to have subclinical hypothyroidism, and in New Zealand only 0.9% of 427 subjects over the age of 80 were affected. The amount of iodine in the diet may be at least partially responsible for this wide variation. To investigate this possibility, two groups of women over the age of 60, one group in Worcester, Massachusetts, and the other in Reggio Italy, were studied and compared. In the Worcester group, 14% had subclinical hypothyroidism, but only 0.6% of the Reggio group was afflicted. The iodine intake was markedly higher in the Worchester group, and 50% of the patients were found to have subtle defects in organification. Another consideration is the extent of medical follow-up and screening by physicians within a community. Obviously, if patients have TSH levels checked periodically and abnormal values treated, the prevalence of subclinical hypothyroidism will be reduced considerably.
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