Hyperthyroidism and Diabetes
Hyperthyroidism refers to thyroid hyperfunction and overproduction of thyroid hormones.
Autoimmune Graves’ disease is the most common cause of hyperthyroidism in young people,
especially young women. Graves’ disease accounts for almost 60% of all cases of
hyperthyroidism. Other causes of hyperthyroidism, including toxic goiter and toxic adenoma, are
more common in older individuals.
Diabetes is more likely to occur among people with hyperthyroidism, and people with
hyperthyroidism are often glucose intolerant.
Symptoms of hyperthyroidism include:
 Weight loss
 Heat intolerance and sweating
 Heart palpitations
 Anxiety
 Tremors
 Fatigue
 Weakness
 Insomnia
 Irritability
 Increased appetite
 Frequent urination
 Muscle weakness
 Alopecia
 Hyperactivity
 Impaired concentration
 Diarrhea
 Pruritis
 Oligomenorrhea (women)
 Amenorrhea (women)
 Erectile dysfunction (men)
Large multinodular goiters can result in dysphagia, respiratory distress, tachycardia, a widened
pulse pressure, and atrial fibrillation.
Autoimmune thyroid disease often occurs with type 1 diabetes because of the alteration of the
immune system and pathological reaction against self-antigens.
Some research has found that patients being treated for Graves’ disease are almost twice as likely
to develop type 2 diabetes and are less likely overweight or with a family history of diabetes,
compared to individuals with normal thyroid function. The pathogenesis of the association
between hyperthyroidism and type 2 diabetes is complex, involving the development of insulin
resistance and metabolic derangement.
Excessive thyroid hormones increase the amount of glucose put out by the liver via
gluconeogenesis and stimulate sympathetic activity in the liver. In hyperthyroidism, rapid
glucose absorption occurs from the intestine. The increased levels of growth hormone and
catecholamines that occur with hyperthyroidism also may contribute to insulin resistance.
Diabetes does not develop unless the pancreatic beta cells fail to act normally and counter the
insulin resistance.
It is important to carefully consider the diagnosis of glucose intolerance needs among people
with hyperthyroidism. Glycemic control often will improve with treatment of thyrotoxicosis. It
also is necessary to rule out hyperthyroidism among people with diabetes and unexplained
worsening hyperglycemia.
Poor glycemic control and hyperthyroidism can mimic each other. Weight loss, increased
appetite, and fatigue can result from both conditions. Diabetic nephropathy and hypothyroidism
both result in edema, fatigue, pallor, and weight gain. To further complicate the diagnostic
process, poorly controlled diabetes may produce changes in thyroid function tests that occur in
nonthyroidal illnesses. Typical changes include a low serum T3 because of impaired
extrathyroidal T4-to-T3 conversion, a low serum T4 because of decreased protein binding, and
an inappropriately low serum thyroid-stimulating hormone concentration.
Some young women with type 1 diabetes develop postpartum thyroiditis, becoming hyperthyroid
for a period of time and then swinging into hypothyroidism. Approximately 30% will not recover
from the hypothyroid phase and will require thyroxine replacement.
Achieving normal thyroid function can improve glucose tolerance, while treating diabetes can
make it easier to control hyperthyroidism. Severe hyperglycemia can falsely decrease blood
levels of T3 and T4.
Antithyroid drugs, including methimazole or propylthiouracil, are used to achieve euthyroidism.
Beta-blockers are sometimes necessary to improve symptoms of sympathetic activation, but
these drugs may mask symptoms of hypoglycemia. Graves’ orbitopathy (bulging of the eyes)
usually is treated with steroids, but steroids cause hyperglycemia. The progression of orbitopathy
usually is well controlled with selenium administration, but long-term selenium administration
increases the risk of developing type 2 diabetes. Radioactive iodine, which is absorbed by the
thyroid cells only, is the most widely recommended therapy for permanent treatment of
hyperthyroidism. Occasionally, surgery to remove part of the thyroid gland is recommended.
It is necessary to avoid thiazolidinedione drugs, commonly used to increase insulin sensitivity,
because it appears to worsen thyroid ophthalmopathy.
References and recommended readings
Diabetes and your thyroid. Diabetes New Zealand Web site.
https://www.diabetes.org.nz/about_diabetes/complications_of_diabetes/thyroid. Accessed May
19, 2014.
Hyperthyroidism. Diapedia Web site. http://www.diapedia.org/other-types-of-diabetesmellitus/hyperthyroidism. Accessed May 19, 2014.
Nordqvist C. What is an overactive thyroid? What is hyperthyroidism? Medical News Today
Web site. http://www.medicalnewstoday.com/articles/9153.php. Published March 4, 2012.
Updated April 2, 2014. Accessed May 19, 2014.
Quick B. Hyperthyroidism and diabetes. Health Central Web site.
http://www.healthcentral.com/diabetes/c/110/162428/hyperthyroidism-diabetes/. Published
August 19, 2013. Accessed May 19, 2014.
Wu P. Thyroid disease and diabetes. Clinical Diabetes. 2000;18(1).
http://journal.diabetes.org/clinicaldiabetes/v18n12000/pg38.htm. Accessed May 19, 2014.
Contributed by Elaine Koontz, RDN, LD/N
Review Date 5/14
D-0687