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  WEIGHT GAIN IN GRAVES' DISEASE
Interpretation of this information is best left to medical professionals trained to do so, as there may be factors the layman is unaware of that make any conclusions we draw from reading these abstracts misleading or erroneous.  Please talk to your doctor if you have any questions.

Link out:  Fatigue, Weight Gain, and the Thyroid (or is the thyroid why I am so tired and can't lose weight)
Merril W. Edmonds MD, FRCP(C)--Endocrinologist, London Health Sciences Centre, for Thyroid Foundation of Canada

Abstracts:

Is excessive weight gain after ablative treatment of hyperthyroidism due to inadequate thyroid hormone therapy?

Tigas S, Idiculla J, Beckett G, Toft A.

Endocrine Unit, Royal Infirmary, Edinburgh, Scotland.

There is controversy about the correct dose and form of thyroid hormone therapy for patients with hypothyroidism. Despite restoration of serum thyrotropin (TSH) concentrations to normal, many patients complain of excessive weight gain. We have compared weight at diagnosis of hyperthyroidism with that when euthyroid, evidenced by a stable, normal serum TSH concentration, with or without thyroxine (T4) replacement therapy, in patients treated with an 18-month course of antithyroid drugs (43 patients), surgery (56 patients), or 13I (34 patients) for Graves' disease. In addition, weights were recorded before and after treatment of 25 patients with differentiated thyroid carcinoma by total thyroidectomy, 131I, and long-term T4 suppressive therapy, resulting in undetectable serum TSH concentrations. Mean weight gain in patients with Graves' disease who required T4 replacement therapy following surgery was significantly greater than in those of the same age, sex, and severity of hyperthyroidism rendered euthyroid by surgery (3.9 kg) (p < 0.001) or at the end of a course of antithyroid drugs (4.1 kg) (p < 0.001). Weight gain was similar in those requiring T4 replacement following surgery or 131T therapy (10.4 versus 10.1 kg). In contrast, ablative therapy combined with suppression of TSH secretion by T4 in patients with differentiated thyroid carcinoma did not result in weight gain. The excessive weight gain in patients becoming hypothyroid after destructive therapy for Graves' disease suggests that restoration of serum TSH to the reference range by T4 alone may constitute inadequate hormone replacement.

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Postgrad Med J 1993 Feb;69(808):107-11

Overweight--a common problem among women treated for hyperthyroidism.

Jansson S, Berg G, Lindstedt G, Michanek A, Nystrom E.

Department of Surgery, Sahlgrenska Hospital, University of Goteborg, Sweden.

We sent out a questionnaire to 112 women treated for diffuse toxic goitre 2-5 years earlier to evaluate the prevalence of problems with overweight after the disease. Of 87 responders, about 50% (irrespective of surgical or radioiodine treatment) reported weight problems, and we randomly selected 40 of these women (20 with and 20 without reported weight problems) for a clinical follow-up (32 appearing). At the follow-up examination (mean 4 years after treatment for hyperthyroidism), 27 women had a higher weight than their estimated premorbid weight. The weight gain correlated with the estimated premorbid body mass index (BMI; P < 0.005), indicating that excess weight gainers may have had a premorbid problem now exaggerated in the post-hyperthyroid period. However, many women with a BMI within the limits stated to be ideal (21-25 kg/m2) also showed dramatic increases in weight. In contrast, the average middle-aged woman in our region did not appear to have gained in weight during a corresponding time period as judged from a longitudinal population study. Women with reported weight problems (mean weight increase 15.6%, n = 16) did not differ from women without (mean weight increase 6.7%, n = 16) as regards pretreatment hormone levels, method of treatment, (change of) smoking habits or post-treatment levothyroxine administration, or in serum concentrations of thyroid hormones, thyrotrophin, cortisol, procollagen-III-peptide, cholesterol, HDL cholesterol or triglycerides. Women with hyperthyroidism should be informed about the risk of gaining weight after therapy and given early support as to dietary and lifestyle change.

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Clin Endocrinol (Oxf) 2001 Aug;55(2):233-9

Weight gain following treatment of hyperthyroidism.

Dale J, Daykin J, Holder R, Sheppard MC, Franklyn JA.

Departments of Medicine and Statistics, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK.

OBJECTIVE: Patients frequently express concern that treating hyperthyroidism will lead to excessive weight gain. This study aimed to determine the extent of, and risk factors for, weight gain in an unselected group of hyperthyroid patients. DESIGN AND SUBJECTS: We investigated 162 consecutive hyperthyroid patients followed for at least 6 months. Height, weight, clinical features, biochemistry and management were recorded at each clinic visit. RESULTS: Documented weight gain was 5.42 +/- 0.46 kg (mean +/- SE) and increase in BMI was 8.49 +/- 0.71%, over a mean 24.2 +/- 1.6 months. Pre-existing obesity, Graves' disease causing hyperthyroidism, weight loss before presentation and length of follow-up each independently predicted weight gain. Patients treated with thionamides or radioiodine gained a similar amount of weight (thionamides, n = 87, 5.16 +/- 0.63 kg vs. radioiodine, n = 62, 4.75 +/- 0.57 kg, P = 0.645), but patients who underwent thyroidectomy (n = 13) gained more weight (10.27 +/- 2.56 kg vs. others, P = 0.007). Development of hypothyroidism (even transiently) was associated with weight gain (never hypothyroid, n = 102, 4.57 +/- 0.52 kg, transiently hypothyroid, n = 29, 5.37 +/- 0.85 kg, on T4, n = 31, 8.06 +/- 1.42 kg, P = 0.014). This difference remained after correcting for length of follow-up. In the whole cohort, weight increased by 3.95 +/- 0.40 kg at 1 year (n = 144) to 9.91 +/- 1.62 kg after 4 years (n = 27) (P = 0.008), representing a mean weight gain of 3.66 +/- 0.44 kg/year. CONCLUSION: We have demonstrated marked weight gain after treatment of hyperthyroidism. Pre-existing obesity, a diagnosis of Graves' disease and prior weight loss independently predicted weight gain and weight continued to rise with time. Patients who became hypothyroid, despite T4 replacement, gained most weight.

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Am J Med 1984 Jun;76(6):963-70

Long-term weight regulation in treated hyperthyroid and hypothyroid subjects.

Hoogwerf BJ, Nuttall FQ.

Body weight regulation after treatment was studied in 87 hyperthyroid and 18 hypothyroid subjects. Mean body weight was 83.9 percent of the premorbid weight at the time of initial treatment for hyperthyroidism and 102.5 percent at 96 months following treatment. Mean (+/- SD) post-treatment weight difference from baseline was 3.4 +/- 18.6 pounds at 96 months (n = 44). Early weight gain was greatest in subjects in whom thyroxine values normalized quickly. Hyperthyroid subjects from whom a body mass index could be calculated (n = 45) were divided into two groups. The obese group had a greater mean weight loss (35.2 +/- 15.0 pounds versus 21.2 +/- 9.9 pounds, p less than 0.001) and a lower weight (percent of baseline weight) at the time of treatment for hyperthyroidism (81.6 +/- 7.7 percent versus 86.0 +/- 5.1 percent, p less than 0.05). Subjects with thyroxine levels of 20 micrograms/dl or more had higher premorbid body weights and greater weight loss from baseline than subjects with thyroxine values below 20 micrograms/dl. Hypothyroid subjects showed a small decline in mean body weight over the first six months of treatment but returned to pretreatment weight by 24 months. In the absence of significant metabolic derangement, body weight is regulated within narrow limits over many years. Effective treatment of hyperthyroidism is accompanied by weight gain.

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The Journal of Clinical Endocrinology & Metabolism 83: 4269-4273, 1998

Body composition changes in nine adults with hyperthyroidism were determined with dual energy x-ray absorptiometry and computed tomography at diagnosis and after 3 and 12 months of euthyroidism achieved by surgery, antithyroid drugs, or treatment with radioiodine. Mean body weight was 67.6 kg at diagnosis and increased 2.7 kg (P = 0.06) and 8.7 kg (P < 0.001) after 3 and 12 months of euthyroidism, respectively. Basal metabolic rate decreased from 2087 Cal/24 h at diagnosis to 1601 Cal/24 h at 12 months (P = 0.001), whereas reported energy intake dropped from 3244 to 2436 Cal/24 h (P = 0.01). According to dual energy x-ray absorptiometry, body fat was unchanged at 3 months, but increased by 5.3 kg (P < 0.0001) at 12 months. Fat-free mass increased 2.7 kg (P = 0.003) at 3 months and 3.5 kg (P < 0.0001) at 12 months. Changes in bone mineral content and density did not reach significance. According to computed tomography, skeletal muscle plus skin areas increased by 11% (trunk) and 18% (thigh) at 3 months and by 17% (trunk) and 25% (thigh) at 12 months. There was no increase in sc adipose tissue (AT) at 3 months, but at 12 months this AT depot increased by 15% (thigh) and 33% (trunk). Intraperitoneal AT showed a borderline significant increase by 28% (P = 0.08) at 3 months and by 40% (P = 0.015) at 12 months. Areas of visceral organs and bone tissue of femur did not change significantly during the study. It is concluded that during early recovery from hyperthyroidism, priority is given to the replenishment of skeletal muscles and ip AT, whereas sc AT is increased at a later stage.

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The Journal of Clinical Endocrinology & Metabolism, April 1997, p. 1118-1125
0021-972X/97/$03.00+0
The Endocrine Society
Vol. 82, No. 4

Resting Energy Expenditure is Sensitive to Small Dose Changes in Patients on Chronic Thyroid Hormone Replacement

Hana Al-Adsani, L. John Hoffer, and J. Enrique Silva
Division of Endocrinology (H.A-A., J.E.S.), Department of Medicine, Jewish General Hospital, McGill University, Montreal, H3T 1E2; McGill Nutrition and Food Science Centre (L.J.H.), Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada H3A 1A1

We have investigated the effects of modifying the dose of thyroxine on resting energy expenditure (REE) and on the thermic effect of glucose (TEG) in 9 randomly recruited patients on chronic treatment with this hormone. The initial dose was changed twice in each patient at 6-8 wk intervals, aiming to have a normal, a slightly reduced, and a slightly elevated serum TSH concentration. A total of 27 dose points for each measured variable (3 per patient) were gathered. Dose changes were monitored with serum free T4, T3, and TSH. At the end of each dose period, low density lipoprotein and high density lipoprotein cholesterol, triglycerides, angiotensin converting enzyme, and sex hormone binding globulin were also measured, along with a systematic assessment of symptoms and signs. The investigators involved in the measurements were blinded to the dose of T4. Serum free T4 and TSH significantly correlated to the dose in each patient and in the whole group, whereas serum T3 levels were minimally affected by the dose and did not correlate with it, with free T4 or with TSH. This latter was below normal on 9 occasions, normal in 12, and above normal in 6. Serum free T4 and T3 remained within the normal range on all except 2 occasions. REE and TEG were normalized to fat-free mass (FFM). In each patient there was a significant negative correlation between REE and TSH. This correlation was maintained when all data were pooled (r2 = 0.64; P < 0.001). Also, initial REE and its change between the highest and the lowest thyroxine dose were significantly correlated with, respectively, initial serum TSH (r2 = 0.85; P < 0.001) and the change in serum TSH between the highest and the lowest dose of T4 (r2 = 0.67; P < 0.0065). REE decreased approximately 15% when TSH increased between 0.1 and 10 mU/L. In 6 of the 9 patients, TEG increased with the reduction of the dose, and higher values were associated with higher TSH levels but without reaching statistical significance (F = 2.852, P = 0.077). None of the other indices were significantly affected by the changes in dose. These results indicate that, in patients on chronic treatment with thyroxine, REE is significantly influenced by the dose of this hormone in a dose range encompassing serum TSH concentrations that are considered acceptable in the management of hypothyroid patients. In the absence of physiological or behavioral compensations, these changes in REE may be clinically relevant. (The Journal of Clinical Endocrinology & Metabolism 82: 1118-1125, 1997)

See also:  Discussion of weight control issues with Graves' Disease, including my personal experience.

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