iThyroid.com

Vitamin A deficiency has been shown to increase T3 and this is further increased by an additional deficiency of iodine. "In the A- and A-I- groups, blood levels of retinol fell to one tenth of the control mean and circulating concentrations of total and free T4 and T3 increased significantly. This biochemical hyperthyroidism contrasted with the maintenance of normal TSH plasma values, suggesting a generalized peripheral refractoriness to thyroid hormones." vitamin A deficiency causes hyperT.doc

The conversion of beta carotene into vitamin A is driven by thyroid hormone. In hyperthyroidism, beta carotene is converted rapidly into vitamin A (which I believe indicates a deficiency of A), while in hypothyroidism, beta carotene conversion to A is markedly decreased, resulting sometimes in a yellowish tint to the skin of a hypo who is consuming beta carotene rich foods. JJ

The following study shows that copper deficiency results in higher liver concentrations of vitamin A (retinol) and lower blood levels of vitamin A, suggesting that "a copper-deficient diet may cause defective transport of vitamin A from liver to blood." 

 

Title

Modification of vitamin A metabolism in rats fed a copper-deficient diet.

Author

Rachman F; Conjat F; Carreau JP; Bleiberg-Daniel F; Amedee-Manesme O

Address

INSERM U 56, Universit´e Paris-Sud, H^opital d'Enfants, Bic^etre, France.

Source

Int J Vitam Nutr Res, 57(3):247-52 1987

Abstract

Title

[Beta-carotene, vitamin A and carrier proteins in thyroid diseases]

Author

Aktuna D; Buchinger W; Langsteger W; Meister E; Sternad H; Lorenz O; Eber O

Address

Internen Abteilung, Krankenhauses der Barmherzigen Br¨uder Graz-Eggenberg.

Source

Acta Med Austriaca, 20(1-2):17-20 1993

Abstract

The conversion of beta-carotene (provitamin A) to 2 molecules of vitamin A (retinol) is accelerated by thyroxine and hyperthyroidism, respectively. The characteristic yellow tint of the skin in hypothyroidism is due to hyper-beta-carotenemia. Both in hyper- and hypothyroidism in a retinol deficiency has been observed in literature. In a series of 36 patients (16 hyper-, 8 hypo-, and 12 euthyroid) serum samples were analyzed for retinol and beta-carotene levels (high pressure liquid chromatography) as well as retinol binding protein (radial immune diffusion), prealbumin (nephelometry), and serum zinc values (atomic absorption spectrometry) were established. The beta-carotene serum level in the hypothyroid group (mean 1.1 microgram/ml) was significantly higher (p < 0.05) in relation to euthyroid controls (0.6 microgram/ml), the hyperthyroid group showed significantly lower values (0.3 microgram/ml). RBP and prealbumin concentrations were significantly lower (p < 0.05) in hyperthyroid as against eu- and hypothyroid patients. Surprisingly, in all 3 groups the retinol levels were not significantly different, although the hyperthyroid group was slightly lower (0.6 microgram/ml) than the mean value of 0.7 micrograms/ml in the other groups. A vitamin A and protein rich food, customary in Central Europe, seems to rule out any vitamin A deficiency both in hyper- and hypothyroidism. However, the beta-carotene values are significantly higher in hypothyroidism, while in hyperthyroidism they were lower. As intrahepatic zinc content plays an important role in the synthesis of RBP and its secretion together with retinol, we also analyzed this component: The serum zinc levels in hyperthyroid patients were clearly higher (79.1 micrograms/dl) than in the hypothyroid group with 57 micrograms/dl (p < 0.05).

The following study indicates that hyperthyroid cats have a 30% high level of vitamin A  (retinol) and a 30% lower level of vitamin E (alpha-tocopherol) than normal cats.

 

Am J Vet Res 1993 Apr;54(4):563-9

Comparison of taurine, alpha-tocopherol, retinol, selenium, and total triglycerides and cholesterol concentrations in cats with cardiac disease and in healthy cats.

Fox PR, Trautwein EA, Hayes KC, Bond BR, Sisson DD, Moise NS

Department of Medicine, Animal Medical Center, New York, NY 10021.

Epidemiologic relations were evaluated between plasma concentrations of nutrients and cardiovascular diseases. A total of 220 cats were assessed: 144 cats with noninduced acquired heart disease and 76 clinically normal cats. Plasma was assayed for taurine, alpha-tocopherol, selenium, retinol, and total cholesterol and triglycerides concentrations. Cardiovascular disease groups included dilated cardiomyopathy (n = 53), left ventricular hypertrophy (n = 28), hyperthyroidism (n = 11), and uncertain classification (n = 52). In cats with dilated cardiomyopathy, mean plasma taurine concentration was the lowest of that in cats of any group, being only 38% of the value in healthy cats; females had less than half the mean value of males. Tocopherol concentration was 20% lower than normal, and retinol concentration was 40% higher than normal. Total cholesterol concentration was 36% lower than normal. Triglycerides concentration was higher in these cats than in any other group--twice the value recorded in healthy cats and 67% higher than that in hyperthyroid cats. In cats with hypertrophic cardiomyopathy, almost 15% had mean plasma taurine concentration < 30 mumol/L. Retinol concentration was 15% higher, and triglycerides concentration was 54% higher than normal. Approximately 27% of hyperthyroid cats had mildly decreased plasma taurine concentration. Hyperthyroid cats had the lowest tocopherol and cholesterol values; both were at least 30% lower than normal. Retinol concentration was 30% higher than normal. Approximately 14% of cats with uncertain classification had mildly decreased plasma taurine concentration. Plasma retinol and triglycerides concentrations were higher than normal in 25 and 38% of these cats, respectively.

 

Acta Med Austriaca 1983;10(2-3):71-3

t

[Vitamin A and carotene in thyroid diseases].

[Article in German]

Smolle J, Wawschinek O, Hayn H, Eber O

From 190 goitrous patients (106 euthyroid, 53 hyperthyroid, 31 hypothyroid) serum levels of vitamin A and carotene were obtained. The serum levels of vitamin A were significantly decreased in both hyperthyroidism and hypothyroidism, the serum levels of carotene in hypothyroidism only. Remarkably, vitamin A levels almost never drop to subnormal values in hyperthyroidism. There is evidence, that a sufficient dietary protein supply enables the liver cell to produce enough amounts of retinol binding protein and prealbumin to overcome the increased clearance observed in hyperthyroid conditions.

 

Experientia Suppl 1983;44:264-97

Vitamin A-deficiency impairs the normal mannosylation, conformation and iodination of thyroglobulin: a new etiological approach to endemic goitre.

Ingenbleek Y

This study was undertaken in order to validate the hypothesis that vitamin A-deficiency alters the structure of thyroglobulin (Tg). For that purpose, four groups of 20 Sprague-Dawley rats were submitted during two months to varying dietary conditions, namely a control diet (C+), a vitamin A-deficient diet (A-), an iodine-deficient diet (I-) and a diet characterized by the association of both deficiencies (A-I-). Both the conventional parameters of thyroid function, the intracellular steps of Tg glycosylation and iodination were analyzed. In the A- and A-I- groups, blood levels of retinol fell to one tenth of the control mean and circulating concentrations of total and free T4 and T3 increased significantly. This biochemical hyperthyroidism contrasted with the maintenance of normal TSH plasma values, suggesting a generalized peripheral refractoriness to thyroid hormones. In both A- and A-I- groups, thyroid cytosol 3H-RPM (retinyl-phosphate-mannose) and 3H-mannose incorporation into the core of the 12S-Tg and 19S-Tg species were reduced by 40-50%. In contrast, cytosolic concentrations of 3H-DPM (dolichyl-phosphate-mannose) rose, suggesting that the N-glycosylation pathways are affected in opposite direction. The sedimentation coefficient in sucrose gradient of the purified dimeric 125I-19S-Tg after guanidine 6M and dithiothreitol denaturation showed that most of the A- Tg molecules were transformed into monomeric 12S species, implying alterations of both noncovalent and covalent bonds. Finally, the radiochromatogram of 125I-iodothyronines recovered after Tg pronase digestion revealed a significant increase in the mono- (MIT) and diiodothyronine (DIT) fractions in contrast with a significant decrease in the T3 and T4 hormonal compounds. These findings are consistent with the view that vitamin A-depletion impairs the endogenous RPM synthesis and, therefore, the normal Tg 0-mannosylation. The growing peptide is characterized by steric hindrance, leading to abnormal closure of disulphide bonds, reduced MIT-DIT coupling reactions and depressed generation of physiologically active thyroid hormones. pure iodine deficit (I-) induces no effects on the above-mentioned glycosylation reactions, but iodine shortage superimposed on preexisting vitamin A-deficit (A-I-) aggravates the Tg dysmaturation

The following study indicates that the benefits of vitamin A supplementation on the hyperthyroid state has been "described for a long time."

 

FEBS Lett 1992 Sep 28;310(2):101-5

Retinoic acid decreases retinoic acid and triiodothyronine nuclear receptor expression in the liver of hyperthyroidic rats.

Higueret P, Pallet V, Coustaut M, Audouin I, Begueret J, Garcin H

Laboratoire de Nutrition, ISTAB, Universite Bordeaux I, Talence, France.

Retinoic acid (RA) and triiodothyronine (T3) exert many of their actions by binding to specific nuclear receptors (respectively, RA receptor (RAR) and T3) receptor (TR) belonging to a 'superfamily' of receptors. Some heterologous regulation of these receptors has been shown, and in particular regulation of the maximum binding capacity of TR by either retinol or RA. Now, using hyperthyroidic rats as a model, the effect of RA on binding capacity and on the mRNA levels of TR and RAR was investigated. The results show that the benefit of vitamin A treatment for the hyperthyroidic state, which has been described for a long time, could be the result of a down-heteroregulation of TR by RA, the active metabolite of retinol.