Hypothyroidism And Weight Gain Pdf

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Body weight and overt thyroid dysfunction are associated. Cross-sectional population-based studies have repeatedly found that thyroid hormone levels, even within the normal reference range, might be associated with body weight.

Weight gain is frequently reported after hemithyroidectomy but the significance is recently discussed. Therefore, the aim of the study was to examine changes in body weight of hemithyroidectomized patients and to evaluate if TSH increase within the reference range could be related to weight gain.

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Hypothyroidism: Foods to eat and avoid

According to common perception, hypothyroidism is held responsible for obesity. However, linking them causally is controversial. Overt hypothyroidism is associated with modest weight gain, but there is a lack of clarity regarding subclinical hypothyroidism.

Novel view indicates that changes in thyroid-stimulating hormone TSH could well be secondary to obesity. The increasing prevalence of obesity further confounds definition of normal TSH range in population studies. Thyroid autoantibody status may help in establishing the diagnosis of subclinical hypothyroidism in obesity.

High leptin levels may play a role in the hyperthyrotropinemia of obesity and also increase susceptibility to thyroid autoimmunity and subsequent hypothyroidism. There is at most a modest effect of L-T4 treatment in overt hypothyroidism in inducing weight loss; benefit in subclinical hypothyroidism is not established with no data supporting thyroid hormone use in euthyroid obese patients.

Obesity and hypothyroidism are two common clinical conditions that have been linked together closely. The link has become more relevant in the context of an unprecedented rise in the prevalence of obesity worldwide. Obesity is generally regarded by patients as being secondary to thyroid dysfunction.

Recent data have also disclosed a relation between obesity and thyroid autoimmunity with the adipocyte hormone leptin appearing to be the key factor linking these two conditions. In this article, we will review the intriguing relationship between obesity and hypothyroidism and the consequent clinical implications.

Body composition and thyroid hormones appear to be closely related. Thyroid hormones regulate basal metabolism, thermogenesis and play an important role in lipid and glucose metabolism, food intake and fat oxidation. Hypothyroidism is associated with decreased thermogenesis, decreased metabolic rate, and has also been shown to correlate with a higher body mass index BMI and a higher prevalence of obesity.

It has been further noted that small variations in serum TSH caused by minimal changes in L-T4 dosage during replacement therapy are associated with significantly altered REE in hypothyroid patients. Evidence suggests that slight variations in thyroid function that are within laboratory reference ranges, also contribute to the tendency to gain weight,[ 4 ] although this has not been confirmed by all studies.

An inverse correlation between free T4 fT4 and BMI, even when fT4 remains in the normal range has been reported;[ 3 ] fat accumulation has been associated with lower fT4 and higher TSH levels among slightly overweight euthyroid individuals, thereby resulting in a positive correlation between TSH and the progressive increase in weight with time.

TSH levels are at the upper limit of the normal range or slightly increased in obese children, adolescents, and adults and are positively correlated with BMI. In obese children, the most common abnormality clearly is hyperthyrotropinemia.

Recently, it has also been shown that obese pediatric patients frequently have an ultrasound pattern of the thyroid which is highly suggestive of Hashimoto's thyroiditis. The causes underlying these alterations in thyroid functions are not known.

One theory suggests an increased deiodinase activity leading to a high conversion rate of T4 to T3. This is interpreted as a defense mechanism in obese subjects capable of counteracting the accumulation of fat by increasing energy expenditure. The main action of leptin is to report centrally the amount of fat, leading to a decrease in appetite and food intake. Leptin also enhances the activity of deiodinases. The hyperthyrotropinemia of obese patients was found to revert after weight loss induced either by bariatric surgery or by hypocaloric diet.

The link between obesity and the risk of autoimmune thyroid dysfunction AITD , which is the main cause of hypothyroidism in adults, is a gray area. The prevalence of AITD in obesity has been reported to be This study suggested that obesity is a risk factor for thyroid autoimmunity, thus establishing a link between the main cause of acquired thyroid failure and obesity. Thermogenically active brown adipose tissue BAT is found in adults. Hence, the presence of thermogenically active D2 BAT in an adult is clinically important.

In the recent years, the presence of BAT has been recognized as an important target for treating obesity. The energy homeostasis in the BAT has been found to be affected by a great extent by thyroid hormone signaling. Thyroid hormone signaling, particularly by inducing type II deiodinases, has a cardinal function in brown tissue adipogenesis. D2 increases expression of the gene Ppargc1a by enhancing thyroid hormone signaling, which coactivates thyroid hormone receptors, leading to increased expression of the gene Ucp1.

Dio2 is also upregulated by increased triiodothyronine T3 signaling. These type II deiodinase D2-dependent pathways provide the mature brown adipocyte with its full thermogenic identity. D2 dependent T3 is necessary for BAT to be functional and also for brown adipogenesis as demonstrated by preclinical trials and cell line studies.

Thereby, activation of BAT in adults, specifically through thyroid hormone-mediated pathways, has a potential role in treating obesity. From a clinical perspective, obesity and mild thyroid failure are common diseases and frequently coexist. Clinicians should be particularly alert to the possibility of thyroid dysfunction in obese patients. The problem lies in identifying obese subjects who are affected by mild thyroid hormone deficiency On one hand, raised TSH may be a just a functional consequence of obesity.

On the other hand, thyroid failure, especially the subclinical form, may go undiagnosed in obese patients. The question that emerges is whether an obese patient should be diagnosed as having subclinical hypothyroidism based on an elevated serum TSH level alone. Data suggest that just an elevated serum TSH might not be enough for diagnosing subclinical hypothyroidism in patients with morbid obesity.

Thus, it would seem reasonable to measure circulating plasma levels of thyroid hormones and thyroid autoantibodies in these patients to support a diagnosis of autoimmune thyroid failure. Obese children may show different degrees of alterations pertaining to thyroid function and thyroid ultrasound. Caution is recommended when diagnosing Hashimoto's thyroiditis in these patients. The diagnosis should not be based just upon a pathological ultrasound, without establishing the presence of antithyroid antibodies.

The other important issue is to be unbiased and not attribute all the weight gain to hypothyroidism. We must remember that there is a significant subset of patients who are overtly hypothyroid, yet lean. All said and done there is paucity of data regarding the extent of actual weight gain in hypothyroidism and the amount of weight loss after restoration to euthyroidism with L-T4 treatment.

Limited data available show that contrary to popular belief, treatment of overt hypothyroidism results in only modest weight loss and that too not necessarily in all patients.

It is also very important to note that although thyroid hormones have been frequently used in attempts to induce weight loss in obese euthyroid subjects, there is no indication for their administration to control body weight except in obese hypothyroid subjects.

In the near future, the increasing prevalence of obesity may confound the definition of normal TSH range in population studies. Mild hyperthyrotropinemia could well be secondary to obesity, so thyroid autoantibody status may help in establishing a diagnosis of subclinical hypothyroidism in obesity. There is at the most a modest effect of L-T4 treatment in inducing weight loss in overt hypothyroidism and benefit in subclinical hypothyroidism is not established. There is no indication for L-T4 administration to control body weight except in obese hypothyroid subjects.

Further research is necessary to determine whether subclinical hypothyroidism is causally involved in the development of obesity. The link between leptin, thyroid autoimmunity, and development of subsequent hypothyroidism needs to be studied. It is conceivable that selected thyroid analogs might be a means to improve weight loss by increasing energy expenditure in obese patients with low T3 during continued caloric deprivation. National Center for Biotechnology Information , U.

Indian J Endocrinol Metab. Debmalya Sanyal and Moutusi Raychaudhuri 1. Author information Copyright and License information Disclaimer. Corresponding Author: Dr. E-mail: moc. This article has been cited by other articles in PMC. Abstract According to common perception, hypothyroidism is held responsible for obesity. Keywords: Hyperthyrotropinemia, hypothyroidism, leptin, obesity, thyroid autoimmunity.

Conflicts of interest There are no conflicts of interest. Effects of changes in body weight on carbohydrate metabolism, catecholamine excretion, and thyroid function. Am J Clin Nutr. Dietary-induced alterations in thyroid hormone metabolism during overnutrition. J Clin Invest. Small differences in thyroid function may be important for body mass index and the occurrence of obesity in the population.

J Clin Endocrinol Metab. Biondi B. Thyroid and obesity: An intriguing relationship. Hyperthyrotropinemia in obese children is reversible after weight loss and is not related to lipids. Subclinical hypothyroidism in obese patients: Relation to resting energy expenditure, serum leptin, body composition, and lipid profile. Obes Res. Hum Nutr Clin Nutr. Longhi S, Radetti G. Thyroid function and obesity. J Clin Res Pediatr Endocrinol. Int J Obes Lond ; 33 —6. Changes in lifestyle improve body composition, thyroid function, and structure in obese children.

J Endocrinol Invest. Raised serum TSH levels in patients with morbid obesity: Is it enough to diagnose subclinical hypothyroidism? Eur J Endocrinol. Investigations of thyroid hormones and antibodies in obesity: Leptin levels are associated with thyroid autoimmunity independent of bioanthropometric, hormonal, and weight-related determinants. Hypothyroidism and obesity? Cause or effect.

Saudi Med J. The role of thyroid hormone and brown adipose tissue in energy homoeostasis. Lancet Diabetes Endocrinol.

Is Your Thyroid Making You Gain Weight?

To the great frustration of many of the 27 million Americans with thyroid gland issues, the thyroid has a profound impact on metabolism. Unintended weight gain and weight loss are common, and both can be a daunting challenge to rectify. Although weight may be the most common complaint, clients are at an increased risk of cardiovascular disease and diabetes, underscoring the need to eat a balanced diet and adopt a healthful lifestyle. But since one-half of all people with thyroid disease are undiagnosed and weight changes are a common symptom,1 RDs are in a prime position to spot potential thyroid conditions, make appropriate referrals, and help clients get a timely diagnosis and the treatment they need. This article will provide an overview of thyroid disease, its relationship with cardiovascular disease and diabetes, and the role nutrition plays in maintaining thyroid health.

The diet can have a significant impact on the symptoms of hypothyroidism. Some foods may improve symptoms, while others may make them worse or interfere with medication. The thyroid is a small butterfly-shaped gland in the throat. Having hypothyroidism , or an underactive thyroid, means that this gland produces less of its hormones than the body needs. Below, we explore how the diet affects hypothyroidism symptoms and which foods to eat and avoid. We then offer a 1-week meal plan for omnivores. Treatment usually involves taking a synthetic version, in the form of a daily tablet.

Hypothyroidism vs. Hyperthyroidism: What’s the Difference?

Javascript is currently disabled in your browser. Several features of this site will not function whilst javascript is disabled. Received 16 April Published 23 August Volume Pages — Review by Single anonymous peer review.

Were you recently diagnosed with hypothyroidism? These symptoms are frustrating.

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