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  • 1. Program T Thyroid Support Breakfast ½ cup cottage cheese with 1 cup chopped fruit, ½ c sunflower seeds * Whole grain bran muffin, 1 Tbsp. almond butter, 6 oz. 2% milk or soy milk, ½ oz. protein powder * ¾ cup oatmeal, 1butter pat, ¼ c strawberries, 2 poached eggs * 2 oz. smoked salmon, sliced cucumbers, 2 tsp. cream cheese, ½ whole grain bagel * 4 oz. Sugar free yogurt, 1 organic hard boiled egg, 1 slice whole grain bread * 2 egg white omelet w/rosemary, cooked in 1 butter pat, ¼ cup black beans, 4 slices avocado * 2 organic eggs any style, 1 slice whole grain toast, 3 tablespoons freshly ground flaxmeal * 1 egg omelet with 1 oz. smoked salmon and spinach, 1 slice whole grain bread, 1 butter pat *box will read “hens were fed flaxseeds, and these eggs contain omega 3 fats” Lunch and Dinner 2 oz. turkey white meat, Dijon mustard, 1 slices whole wheat bread, organic spinach salad with 3 tsp. flax oil and vinegar * 3 oz. stir fried fish with snow pea pods, onions bean sprouts, red pepper, ½ cup organic brown rice, 4 slices avocado, 3 tsp. olive oil for cooking * 2 oz. lean London broil, 1 small baked potato, 2 Tbsp. sour cream, Caesar salad (no croutons), 2 Tbsp. Caesar dressing * 2 oz. broiled red snapper, crusted with ¼ c crushed almonds ½ c steamed asparagus, ½ c baked yams, 2 butter pats * Large mixed green salad w/ 3 tsp. Oil and lemon juice, small can of 2 oz. Tuna, chopped yellow and sweet red pepper, 4 Wasa crackers * 2 oz. flank steak or any meat, ½ c green beans with 1 oz. sliced brazil nuts, green salad with flax dressing, ½ c brown rice * 2 oz. broiled mackerel, ½ c steamed green beans or other vegetable, ½ c barley, 2 tsp. flax oil 1
  • 2. Program T Thyroid Support * 2 oz. chicken salad made with2 tsp. sugar-free mayonnaise, ½ c roasted vegetables, spinach salad, 2 tsp. olive oil, ½ whole wheat pita * 2 ounces wood-smoked or broiled salmon with 2 Tbsp. crushed almond crust, ½ cup brown rice vermicelli pasta (Pastariso brand), ½ c tomato sauce w/ extra oregano, thyme, and garlic, grilled leeks, 2 tsp. olive oil * 2 oz. chicken breast with rosemary and 4 pieces sun dried tomato, small baked sweet potato, roasted onions or garlic, spinach salad with 1.5 Tbsp. sesame-tahini dressing * Broiled chicken breast, grilled organic vegetables, 1 fruit * Salmon burger patties made with 3 oz. chopped salmon, onions, dill, an egg, and ¼ cup ground sesame seeds, and sautéed in skillet with 1 Tbsp. butter, 2 cups of sautéed mushrooms , 1 small cob of corn, 1 pat of butter * Albacore tuna broccoli custard made with 1 c. fresh chopped broccoli, 2 oz. tuna, 2 tsp. parmesan cheese, ½ c. whole wheat macaroni shells, 3 tsp. olive oil, 2 Tbsp. lemon juice, seasonings, mixed together and baked at 375ºf for 35 minutes * Gourmet salmon salad made with 2oz. can salmon, 2 tsp. sliced scallions, 1 tsp. sliced radishes, 2 tsp. rice vinegar, 1 tsp. flax oil, 1 tsp. soy sauce, and ¼ tsp. minced ginger root, and ½ c brown rice all placed atop a green salad * Crab and avocado salad made with 1/3 cup chopped celery, 2 oz. cooked fresh crabmeat, 1 Tbsp. mayonnaise, 1 tsp. cumin, ½ tsp. turmeric, 1 Tbsp. capers, juice of ½ lemon, ½ medium avocado, seasonings to taste, and 1 bunch watercress with stems removed, 4 Wasa crackers * Sautéed 2 oz of sausage, ½ cup red or green pepper, ¼ cup chopped onion, ½ cup chopped zucchini, served in a small whole wheat tortilla Snacks small fruit and an ounce of cheese, 1 ounce of cheese and 60 calories of crackers, 1 ounce of meat and 1 slice of bread, 1 hard boiled egg and 60 calories of crackers, dried Kelp. Limit 2
  • 3. Program T Thyroid Support Sugar, wheat, soft drinks, alcohol, processed meats, refined foods, as well as goitrogens rich foods such as turnips, cabbage, mustard, cauliflower, broccoli, cassava root, soybeans, peanuts, and millet. Goitrogens block iodine utilization in the thyroid. Completely avoid: pesticides, hydrogenated oils, safflower, sunflower, corn oils, aspartame Suggestions and Goals Research suggests that 10-20% of the population has undiagnosed thyroid problems. Orthodox physicians often rely purely on blood tests to determine thyroid function. Cutting- edge practitioners also look at signs of hypothyroid that include a morning underarm temperature under 97 degrees, constipation, depression, weight gain, and low energy. Many low thyroid patients on replacement therapy feel overall improvements when thyroid hormone is switched from Synthroid (synthetic T4) to Armour thyroid (natural mixture of T3 and T4.) The thyroid gland makes both forms of the hormone, and it is T3 that is responsible for the fat burning and other metabolic stimulating effects of thyroid. Selenium is necessary to run the enzyme in the body that converts T4 to T3, but even with adequate selenium nutriture this enzyme may not give the body optimal T3 levels. Hypothyroidism is one of the most important areas for carnitine supplementation. Those with decreased thyroid function have decreased excretion of carnitine, suggesting they have lower body levels and decreased manufacture of this key fat burning nutrient. Higher levels of thyroid hormone also leads to increased carnitine loss as well. Those with low thyroid function benefit from carnitine supplements. Hypothyroid patients also have elevated levels of fats in their blood which carnitine will lower. 3
  • 4. Program T Thyroid Support Supplements Carnitine 1,000-4,000 mg (½ hour before breakfast and lunch) Thyroid Glandular 100-600 mg CoQ10 30-120 mg B complex 50 mg Magnesium 400-600 mg Zinc 25-50 mg Iodine 100-300 mcg Selenium 200-300 mcg GLA 240 1-2 capsules EPA/DHA 500-2,000 mg Vitamin A 5,000-10,000 IUs Vitamin E 400 IUs Vitamin C 1,000 mg Myrrh 20-60 mg and up Sage 40-60 mg and up 4
  • 5. Program T Thyroid Support Research Review Environmental Influences The present study was conducted to examine the effect of organochlorine (Heptachlor, Benzene hexachloride (BHC)), organophosphorus (Malathion, Monitor) and pyrethroid (Karate, Talstar) insecticides on the thyroid secretory function in rats. Among organochlorine and organophosphorus insecticides, treatment with BHC and Malathion, respectively, led to a significant decrease (P 0.01) in serum concentration of T3 and T4. Administration of BHC and Malathion also increased (P 0.01) TSH secretion. Treatment with both of the pyrethroid insecticides similarly induced significant suppression (P 0.01) of serum T3 and T4 levels, and concomitant stimulation (P 0.01) of TSH concentrations. The T4/T3 ratio was decreased (P 0.05) in rats treated with Karate but not with any other insecticide. These data indicate that immense care is warranted in the use of insecticides, because they not only affect the liver, kidney and other organs but also may alter the activity of the endocrine glands.1 Antioxidants and Free Radicals In this study, the effect of different levels of thyroid hormone and metabolic activity on low density lipoprotein (LDL) oxidation was investigated. Thus, in 16 patients with hyperthyroidism, 16 with hypothyroidism, and 16 age- and sex-matched healthy normolipidemic control subjects, the native LDL content in lipid peroxides, vitamin E, beta-carotene, and lycopene, as well as the susceptibility of these particles to undergo lipid peroxidation, was assessed. Hyperthyroidism was associated with significantly higher lipid peroxidation, as characterized by a higher native LDL content in lipid peroxides, a lower lag phase, and a higher oxidation rate than in the other two groups. This elevated lipid peroxidation was associated with a lower LDL antioxidant concentration. Interestingly, hypothyroid patients showed an intermediate behavior. In fact, in hypothyroidism, LDL oxidation was significantly lower than in hyperthyroidism but higher than in the control group. Hypothyroidism was also characterized by the highest beta-carotene LDL content, whereas vitamin E was significantly lower than in control subjects. In conclusion, both hypothyroidism and hyperthyroidism are characterized by higher levels of LDL oxidation when compared with normolipidemic control subjects.2 The levels of alpha-tocopherols and gamma-tocopherols in the thyroid tissue of patients with papillary carcinoma and the level of gamma-tocopherol in the thyroid tissue of patients with malignant lymphoma were elevated compared with those in normal thyroid tissues. The level of coenzyme Q was reduced in the thyroid tissue of patients with Graves' disease and follicular and papillary thyroid carcinomas. These findings imply that vitamin E and coenzyme Q as scavengers play some role in thyroid follicular cell hyperfunction or dysfunction.3 Magnesium Changes in magnesium metabolism, along with those in sodium, were investigated in 17 patients with Graves' disease (14 females and 3 males, mean +/- SD, 44.8 +/- 12.2 years) and their relationship to plasma levels of thyroid hormones were assessed before and after treatment. Each patient was studied in hyperthyroid state and euthyroid state after treatment. Each patient was studied in hyperthyroid state and euthyroid state after treatment with methimazole. Treatment with methimazole increased the magnesium concentration both in erythrocytes and in serum but both urinary output and fractional excretion of magnesium decreased significantly. Urinary excretion of sodium also decreased with treatment (P 0.05), but only changes in indices 5
  • 6. Program T Thyroid Support of magnesium metabolism (decrease in renal fractional excretion, rise in serum level) correlated significantly with those of the thyroid functions with treatment. These observations clearly indicate that in Graves' disease, the magnitude of magnesium metabolism alteration is closely related to the extent of the increase in thyroid hormones in plasma.4 Zinc In subjects affected by trisomy 21 (Down syndrome), hypothyroidism is the most common endocrinological deficit. Plasma zinc levels, which are commonly detected below the normal range in Down patients, are related to some endocrinological and immunological functions; in fact, zinc deficiency has been shown to impair immune response and growth rate. Aims of this study were to evaluate (1) the role of zinc deficiency in subclinical hypothyroidism and (2) thyroid function changes in Down children cyclically supplemented with zinc sulfate. Inverse correlations have been observed between age and triiodotironine (T3) and between zinc and thyroid-stimulating hormone (TSH); higher TSH levels have been found in hypozincemic patients at the beginning of the study. After 6 mo of supplementation, an improvement of thyroid function was observed in hypozincemic patients. In the second cycle of supplementation, a similar trend of TSH was observed. At the end of the study, TSH significantly decreased in treated hypozincemic subjects and it was no longer different in comparison to normozincemic patients.5 We examined zinc (Zn) status in relation to thyroid function. After measuring serum free 3,5,3'- triiodothyronine (T3) and free thyroxine (T4) in 134 persons, TSH-releasing hormone (TRH) injection test and estimation of Zn status were conducted in persons with low free T3. RESULTS: Thirteen had low levels of serum free T3 and normal T4. Nine of 13 patients had mild to moderate Zn deficiency evaluated by body Zn clearance and increased urinary Zn excretion. After oral supplementation of Zn sulphate (4-10 mg/kg body weight) for 12 months, levels of serum free T3 and T3 normalized, serum rT3 decreased, and the TRH- induced TSH reaction normalized. Serum selenium concentration (Type 1 T4 deionidase contains selenium in the rat) was unchanged by Zn supplementation. Zn may play a role in thyroid hormone metabolism in low T3 patients and may in part contribute to conversion of T4 to T3 in humans.6 Erythrocyte zinc values were significantly lower than normal in hyperthyroidism and higher in hypothyroidism. A significantly higher than normal urinary excretion of zinc was observed in hyperthyroidism. The mean concentrations of plasma and erythrocyte copper were significantly above normal in hyperthyroidism. Plasma selenium levels were significantly lower than normal in hyperthyroidism. The erythrocyte manganese content correlated well with thyroxine and triiodothyronine levels. The results of this study suggest that the metabolism of zinc, copper, manganese, and selenium is abnormal in thyroid diseases.7 Selenium Effects of high dietary selenium supply (range 170-980 micrograms per day) on the metabolism of thyroid hormones were studied in serum of mothers living in 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. It was hypothesized that 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 6
  • 7. Program T Thyroid Support discussed with respect to the safe level of dietary selenium intake, which was estimated to be below 500 micrograms per day.8 Selenium and Iodine Administration of the anti-oxidative trace element selenium is currently being evaluated for its benefits in patients with inflammatory diseases. However, little is known about the risks of selenium. We report on a patient in whom, along with standard therapy, administration of large intravenous doses of selenite for sepsis secondary to pneumonia resulted in development of marked hypothyroidism. In addition, severe iodine deficiency was noted, and supplementation with iodine led to normalization of thyroid function.9 Carnitine Urinary excretion of carnitine and serum concentrations of carnitine, triglyceride, and free fatty acids were measured in 54 hyperthyroid and 13 hypothyroid patients, and the results were compared with those of normal subjects. In hyperthyroid patients urinary excretion of carnitine was highly increased above that of the control subjects. On adequate treatment with antithyroid drug, carnitine excretion was reduced to the normal range, and serum lipids changed in parallel. In contrast, carnitine excretion was markedly reduced in hypothyroid patients. After substitution therapy with thyroid hormones the excretion increased in these patients. This change was associated with a marked reduction of serum triglyceride. There was an inverse correlation between urinary excretion of carnitine and serum triglyceride concentration. Carnitine excretion was significantly correlated with serum thyroxine concentration in hyper- and hypothyroid patients. The results suggest that thyroid hormones play an important role in carnitine metabolism, which in turn influences serum triglyceride metabolism.10 Interferon Treatment Damages Thyroid Metabolism We describe the case of a 48-year-old woman from Thailand diagnosed with chronic hepatitis C, who experienced a suppression of all blood cell counts accompanied by a newly developed clinically manifested autoimmune thyroid disorder after treatment with interferon alpha-2b (INF-alpha) 46 days after beginning of therapy a decrease of platelet, red and white blood cell counts became obvious. Concomitantly we observed an increase of FT4 and FT3 with a totally depressed TSH level 80 days after starting INF-alpha administration. Antibody assessment resulted in detection of high numbers of antithyroid- microsomal antibodies and antithyroglobulin antibodies. Thyroid hormone levels normalized under treatment with methimazole/propylthiouracil within 4.5 months. However, two months after cessation of antithyroid therapy increasing TSH levels and decreasing FT4 levels indicated a new tendency towards a hypothyroid state. CONCLUSION: We classify this case as an interferon-alpha-induced disorder of thyroid function accompanied by myelosuppression. A close monitoring for thyroid dysfunction, e.g. evaluation of TSH-levels before and after administration of INF-alpha is mandatory.11 Red Blood Cell and Plasma Volume Decrease in Hypothyroidism Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was 7
  • 8. Program T Thyroid Support not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H- thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.12 Mitochondrial Membrane Function Proton leak, as determined by the relationship between respiration rate and membrane potential, was lower in mitochondria from hypothyroid rats compared to euthyroid controls. Moreover, proton leak rates diminished even more when hypothyroid rats were fed a diet containing 5% of the lipid content as n-3 fatty acids. Similarly, proton leak was lower in euthyroid rats fed the 5% n-3 diet compared to one containing only 1% n- 3 fatty acids. Lower proton leaks rates were associated with increased inner mitochondrial membrane levels of n-3 fatty acids and a decrease in the ratio of n-6/n-3 fatty acids. This trend was evident in the phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and cardiolipin phospholipid fractions. These results suggest that a significant portion of the effect of thyroid hormone status on proton leak is due to alterations in membrane fatty acid composition, primarily changes in n-3 content. Both the hypothyroid state and dietary effects appear to be mediated in part by inhibition of the Delta6- and Delta5-desaturase pathways.13 Reduced NSAID Toxicity in Hypothyroidism Recent data from animal studies suggest that induced hypothyroidism inhibits the development of liver injury in several animal models, including liver cirrhosis and fulminant hepatic failure in rats, and immune-mediated acute liver injury in mice. The aim of the present study was to determine whether hypothyroidism would likewise prevent acetaminophen-induced hepatic damage in rats. Liver damage was induced by acetaminophen (2 g/kg) administered by gavage to fasting rats as a single dose. Hypothyroidism was induced by methimazole, propylthiouracil, or surgical thyroidectomy and confirmed by elevated serum levels of TSH. Hypothyroidism significantly inhibited acetaminophen-induced liver damage as manifested by the decreased serum levels of liver enzymes, malondialdehyde and blood ammonia, as well as by the higher hepatic glutathione content, in all three groups of hypothyroid rats compared to euthyroid controls (P 0.01). Histopathologic analysis showed significantly less liver necrosis and inflammation in the acetaminophen- treated hypothyroid rats. Oxygen extraction, measured in isolated perfused rat liver preparation, was also reduced in the hypothyroid livers to 42+/-8% compared to 81+/-14% of controls (P 0.01). However, the 8
  • 9. Program T Thyroid Support expression of CYP2E1 in the livers of hypothyroid rats, as measured by western blot analysis, was not decreased compared to control rats. These results suggest that induced hypothyroidism, regardless of the mode of induction, protects rat liver from acetaminophen hepatotoxicity. This effect may be related to hypometabolism of liver cells, but the exact mechanism needs further clarification.14 1. Akhtar N, Kayani SA, Ahmad MM, Shahab M. Insecticide-induced changes in secretory activity of the thyroid gland in rats. J Appl Toxicol 1996;16(5):397-400. 2. Costantini F, Pierdomenico SD, De Cesare D, et al. Effect of thyroid function on LDL oxidation. Arterioscler Thromb Vasc Biol 1998;18(5):732-7. 3. Mano T, Iwase K, Hayashi R, et al. Vitamin E and coenzyme Q concentrations in the thyroid tissues of patients with various thyroid disorders. Am J Med Sci 1998;315(4):230-2. 4. Disashi T, Iwaoka T, Inoue J, et al. Magnesium metabolism in hyperthyroidism. Endocr J 1996;43(4):397-402. 5. Bucci I, Napolitano G, Giuliani C, et al. Zinc sulfate supplementation improves thyroid function in hypozincemic Down children. Biol Trace Elem Res 1999;67(3):257-68. 6. Nishiyama S, Futagoishi-Suginohara Y, Matsukura M, et al. Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency. J Am Coll Nutr 1994;13(1):62-7. 7. Aihara K, Nishi Y, Hatano S, et al. Zinc, copper, manganese, and selenium metabolism in thyroid disease. Am J Clin Nutr 1984;40(1):26-35. 8. Bratter P, Negretti de Bratter VE. Influence of high dietary selenium intake on the thyroid hormone level in human serum. J Trace Elem Med Biol 1996;10(3):163-6. 9. Hofbauer LC, Spitzweg C, Magerstadt RA, Heufelder AE. Selenium-induced thyroid dysfunction. Postgrad Med J 1997;73(856):103-4. 10. Maebashi M, Kawamura N, Sato M, Imamura A, Yoshinaga K. Urinary excretion of carnitine in patients with hyperthyroidism and hypothyroidism: augmentation by thyroid hormone. Metabolism 1977;26(4):351-6. 11. Schmitt K, Hompesch BC, Oeland K, von Staehr WG, Thurmann PA. Autoimmune thyroiditis and myelosuppression following treatment with interferon-alpha for hepatitis C [In Process Citation]. Int J Clin Pharmacol Ther 1999;37(4):165-7. 12. Das KC, Mukherjee M, Sarkar TK, Dash RJ, Rastogi GK. Erythropoiesis and erythropoietin in hypo- and hyperthyroidism. J Clin Endocrinol Metab 1975;40(2):211-20. 13. Pehowich DJ. Thyroid hormone status and membrane n-3 fatty acid content influence mitochondrial proton leak [In Process Citation]. Biochim Biophys Acta 1999;1411(1):192-200. 14. Bruck R, Frenkel D, Shirin H, et al. Hypothyroidism protects rat liver from acetaminophen hepatotoxicity. Dig Dis Sci 1999;44(6):1228-35. 9