Thyroiditis
Anorexia & Thyroiditis
Adaptive changes in metabolism result in decreased energy requirements in AN.
Refeeding requires an understanding of both baseline requirements and metabolic changes that occur during nutritional rehabilitation.
Evaluated changes in fasting and postprandial resting energy expenditure (REE).
Significant increases in both REE and postprandial REE persisted in patients requiring longer hospitalizations.
Energy metabolism in AN adapts to semistarvation by a reduction in fasting REE. With refeeding there is a reversal of this adaptive function, demonstrated by an increase in both fasting and postprandial energy expenditure. The increase in postprandial REE is not related to energy intake or thyroid function.
Schebendach JE et al., The metabolic responses to starvation and refeeding in adolescents with anorexia nervosa. Ann N Y Acad Sci, 817:110-9 1997 May 28.
Cachexia & Thyroiditis
Body composition is a reflection of the metabolic state of the organism. However, because the time course of change in body composition is slower than that of metabolic processes, measurement of body composition offers a unique way of assessing the organism's physiologic status.
The hormonal and immune mediators that control metabolism, and thus body composition, can be divided into 3 categories: day-to-day regulators (insulin and glucagon), life cycle-related hormones (estrogens and androgens, growth hormone, prolactin, thyroid hormones, catecholamines, corticosteroids) and immunologic mediators (the cytokines interleukin-1, tumor necrosis factor, and interleukin-6).
Although the cytokines can clearly drive metabolism and thus body composition in various illnesses, it is not yet clear whether they also play a homeostatic role in the age-related changes in body composition that we now call sarcopenia.
Roubenoff R: Inflammatory and hormonal mediators of cachexia. J Nutr, 127(5 Suppl):1014S-1016S 1997 May.
Alcohol & Thyroiditis
Fetal alcohol
Alcohol can alter both endocrine and immune function in the adult organism. Acting directly on the endocrine glands themselves, and/or at the level of the pituitary or brain, alcohol has been shown to alter secretory activity of most of the endocrine systems that have been studied. Similarly, the association between alcoholism and infections and between alcoholism and certain forms of cancer has long been recognized by clinicians.
Alcohol consumption may, indeed, be associated with immune impairment, independent of nutritional deficiencies, liver disease, or general poor health that may occur.
Our knowledge of the teratogenic effects of alcohol on the developing organism has expanded, that the effects of fetal alcohol exposure on endocrine and immune function of the offspring have begun to receive considerable attention.
Reviewed recent clinical and experimental literature on the effects of fetal alcohol exposure on offspring endocrine and immune development.
Weinberg J: Recent studies on the effects of fetal alcohol exposure on the endocrine and immune systems. Alcohol Alcohol Suppl, 1994, 2:401-9.
Obesity & Thyroiditis
Obesity and metabolic efficiency
Obesity has a strong genetic component, which should be viewed as a predisposition only if certain environmental factors are present. Impaired regulation of both sides of the energy balance equation plays a role in the propensity to gain weight and develop obesity.
Overeating may be induced in susceptible individuals by high dietary fat content, large portion sizes and low meal frequency. Increased metabolic efficiency in the form of a low resting metabolic rate has been identified in pre- and post-obese subjects, and the impact on total energy expenditure may be amplified by a low level of physical activity.
The heterogeneous nature of obesity indicates that different mechanisms, such as changes in the partitioning of fat (due to lipoprotein lipase activity, fat oxidative muscle enzymes) and carbohydrate, and an altered responsiveness of the sympathoadrenal system and thyroid hormones to a positive energy balance, seem to be involved.
Astrup A: Obesity and metabolic efficiency. Ciba Found Symp, 1996, 201:159-68; discussion 168-73, 188-93.
Postnatal Thyroiditis
Energy intake profoundly influences many endocrine axes which in turn play a central role in development. The specific influence of a short period of mild hypothyroidism, similar to that induced by undernutrition, in regulating muscle development has been assessed in piglets during early postnatal life. Hypothyroidism was induced.
During early postnatal development of large mammals, a period of mild hypothyroidism, comparable with that found during undernutrition, induces changes in myofibre differentiation and a down-regulation of cation pumps in skeletal muscle. Such changes would result in slowness of movement and muscle weakness, and also reduce ATP hydrolysis with a concomitant improvement in energetic efficiency.
Harrison AP et al., Role of thyroid hormones in early postnatal development of skeletal muscle and its implications for undernutrition. Br J Nutr, 76(6):841-55 1996 Dec.
Selenium & Thyroiditis
Selenium (1)
In studies evaluating the combined effect of selenium- iodine deficiency and the etiology of endemic myxedematous cretinism in Zaire, it was suggested that selenium supplementation not be done without thyroid supplementation in cases of combined selenium and iodine deficiencies. Selenium deficiency may lower glutathione peroxidase activity in the thyroid gland, which allows hydrogen peroxide produced during thyroid hormone synthesis to be cytotoxic. Selenium supplementation may aggravate the hypothyroidism, by stimulating thyroxine metabolism by the selenoenzyme type I iodothyronine 5'-deiodinase.
"Selenium Deficiency Mitigates Hypothyroxinemia in Iodine-Deficient Subjects," Vanderpas, Jean B., et al, American Journal of Clinical Nutrition Supplement, 1993;57:271S-5S.
Selenium (2)
This study compared two goiter-endemic areas in Zaire and Malawi, for thyroid indices and thiocyanate concentrations. The high frequency of myxedematous cretins seen in Ubangi probably resulted from severe iodine and selenium deficiencies, with thiocyanate overload.
"The Epidemiology of Iodine-Deficiency Disorders in Relation to Goitrogenic Factors and Thyroid-Stimulating-Hormone Regulation," Thilly, Claude-Hector, American Journal of Clinical Nutrition Supplement, 1993;57:267S-70.
Selenium (3)
Selenium deficient rats have low tissue deiodinase activity, and abnormal thyroid hormone metabolism. In conclusion, selenium deficiency decrease T4 conversion to T3 in tissues containing deiodinase-I or deiodinase-II. Inhibition deiodinase activity results in increased plasma T4, and decreased plasma T3 seen in selenium deficient animals. Evaluation of the changes in hormonal status caused by selenium deficiency need to be further elucidated.
"Selenium Deficiency, Thyroid Hormone Metabolism, and Thyroid Hormone Deiodinases," Arthur, John R., et al, American Journal of Clinical Nutrition Supplement, 1993;57:236S-9S.
Selenium (4) - Breast cancer
Within a case-control study of postmenopausal breast cancer patients (n = 99) and matched healthy controls (n = 105), thyroid hormone levels were compared and correlated with toenail selenium concentrations.
Plasma triiodothyronine (T3) was significantly lower in cases (1.4 +/- 0.4 nmol/l) than in controls (1.6 +/- 0.4 nmol/l), and a strong inverse relationship with breast cancer was observed with an odds ratio of 0.17 in the highest compared with the lowest tertile of T3.
Plasma thyroxine and thyroid-stimulating hormone concentrations were similar between cases and controls. Plasma T3 concentration was positively associated with toenail selenium in cases and controls.
Toenail selenium concentrations tended to be lower in cases than in controls, but the differences did not reach statistical significance.
Although the disease process per se may explain the lower plasma T3 concentrations, it is also possible, inasmuch as these patients were in early-stage breast cancer, that selenium status may be influencing T3 levels via changes in the activity of the selenoenzyme type 1 iodothyronine deiodinase.
Strain JJ et al., Thyroid hormones and selenium status in breast cancer. Nutr Cancer, 27(1):48-52 1997.
Selenium (5)
Studied effects of high dietary selenium supply (range 170-980 micrograms per day) on the metabolism of thyroid hormones. (Seleniferous areas of Venezuela.)
Free thyroxine (FT4), free triiodothyronine (FT3) and human thyroid stimulating hormone (hTSH) were found to be within the normal range but a significant inverse correlation was found between the FT3 and selenium.
The activity of hepatic selenoenzyme type I iodothyronine 5'-deiodinase, which catalyzes the production of T3 from T4, becomes depressed at high levels of dietary intake of selenium. The effect is discussed with respect to the safe level of dietary selenium intake, which was estimated to be below 500 micrograms per day.
Braumlitter P: Influence of high dietary selenium intake on the thyroid hormone level in human serum. J Trace Elem Med Biol, 10(3):163-6 1996 Sep.
Zinc & Thyroiditis
Zinc and selenium
Zinc deficiency decreased concentrations of triiodothyronine (T3) and free thyroxine (fT4) in serum by approximately 30% when compared with zinc-adequate controls.
The concentration of thyroxine (T4) in serum was not affected by zinc deficiency. Selenium-deficient rats had lower concentrations of T3 and T4 than selenium-adequate animals.
The concentration of fT4 in serum was not affected by selenium deficiency. The activity of hepatic type I 5'deiodinase was decreased by 67% by zinc deficiency and by 47% by selenium deficiency compared to adequate controls.
Data show that both zinc and selenium deficiency affect the metabolism of thyroid hormones.
Kralik A et al., Influence of zinc and selenium deficiency on parameters relating to thyroid hormone metabolism. Horm Metab Res, 28(5):223-6 1996 May.
Glutathione & Thyroiditis
There are several hypotheses regarding selenium deficiency's effect on iodine metabolism from rat models, and from epidemiologic and experimental studies in humans.
By decreasing intracellular glutathione peroxidase activity, selenium deficiency may increase hydrogen peroxide and lead to thyroid atrophy, which is seen in myxedematous cretins over several weeks.
Selenium deficiency could protect fetal brain T4 supply while preventing neurologic cretinism. This is possible by enhancing thyroid hormone synthesis, and by decreasing peripheral thyroxin (T4 deiodination).
Selenium deficiency may protect against iodine deficiency, by decreasing T4 metabolism and subsequent iodine leakage. By increasing hydrogen peroxide supply and thyroid hormone synthesis, thyroid deficiency may be improved.
"Selenium and the Thyroid: How the Relationship was Established," Corvilain, Bernard, et al, American Journal of Clinical Nutrition Supplement, 1993;57:244S-8S.
Infant feeding & Thyroiditis
Feeding practices were evaluated in children with autoimmune thyroid disease compared to healthy siblings and controlled children. Breast feeding frequency and duration were not different. Analysis revealed an association of soy formula feedings in infancy with autoimmune thyroid disease.
"Breast and Soy Formula Feedings in Early Infancy and the Prevalence of Autoimmune Thyroid Disease in Children", Fort, P., M.D., et al, The Journal of The American College of Nutrition, 1990;9(2):164-167.
Iodine & Thyroiditis
Iodine deficiency is recognized as a major cause of endemic goiter. Iodine supplementation is effective in preventing endemic cretinism, provided it is given before conception, which may help prevent early fetal and infant death.
It is noted that oral iodinated oil has proven effective, with a duration of action of approximately 1 to 2 years. Though this is less than the effect of intramuscular injections, it is acceptable and cheaper.
"Iodine-Supplemented Trials," Pharoah, Peter O.D., American Journal of Clinical Nutrition Supplement, 1993;57:276S-9S. þ 1993, American Society For Clinical Nutrition.
Urticaria & Thyroiditis
Urticaria and angio-oedema
A 60 year old woman affected by Hashimoto's thyroiditis presented with a history of recurring episodes of urticaria and angio-oedema.
A pathogenic relation between Hashimoto's thyroiditis and chronic urticaria/angio-oedema was suspected. However, treatment with L-thyroxine had no influence on the frequency and severity of the cutaneous and mucosal manifestations, which occurred almost daily and required repeated administration of steroids.
The patient therefore underwent total thyroidectomy. Urticaria and angio-oedema completely remitted after surgery; 18 months postoperatively the patient was still asymptomatic.
Amoroso A et al., Hashimoto's thyroiditis associated with urticaria and angio-oedema: disappearance of cutaneous and mucosal manifestations after thyroidectomy. J Clin Pathol, 1997 Mar, 50:3, 254-6.
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