How to Lose Weight With Hypothyroidism

Overcome an underactive thyroid for effective weight loss

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If you have an underactive thyroid, your thyroid has been surgically removed, or you have had radioactive iodine to treat an overactive thyroid, you may struggle with an inability to lose weight. However you ended up with an underactive, inactive, or surgically removed thyroid gland, you may find that, even with prescription drug treatment for your hypothyroidism, you still can’t lose weight—or can’t stop gaining weight—despite your best efforts.

Understandably, it's frustrating. In this situation, it's helpful to understand the factors contributing to difficult weight loss and how you can address them so that you can lose weight with hypothyroidism.

What Makes Weight Loss Difficult for Thyroid Patients?

What thyroid patients need to know is that there are 5 factors that may make it significantly more difficult to lose weight:

Let's explore each one and identify strategies to address them.

Inadequate Thyroid Treatment

For many conventional endocrinologists, the goal of hypothyroidism treatment is to restore you to a thyroid stimulating hormone (TSH) level somewhere within the TSH reference range. At that point, you are considered euthyroid, which means that your thyroid function is normal.

Some studies show, however, that TSH levels in the upper end of the reference range are linked to increased weight, higher body mass index (BMI), and higher rates of obesity. To that end, some physicians aim to keep the TSH level at the mid-point of the reference range, or even lower, in some patients.

A Need for T3

Conventional therapy for hypothyroidism is levothyroxine, a synthetic form of the T4 hormone. Some studies, however, have shown that nutritional deficiencies, genetic defects, and other factors predispose some people to have an increased need for the active thyroid hormone triiodothyronine (T3).

Those studies have shown some weight loss and increase in metabolism in patients who are treated not with levothyroxine alone, but with a T4/T3 combination therapy—such as levothyroxine plus liothyronine (synthetic T3), or natural desiccated thyroid drugs like Nature-throid and Armour that include both T4 and T3.

A Changed Metabolic "Set Point"

Your metabolism works to protect you from starvation, ensure sufficient energy, and to maintain you at what’s known as a “set point,” a particular weight that, like a 98.6-degree body temperature, your body tries to maintain. Initially, as you start to take in too many calories—or your metabolism slows—you will notice a small increase in weight gain. When operating normally, your metabolism will then speed up to burn off extra weight gain, your appetite drops, and your weight returns back to your normal set point.

If your metabolism is chronically slower—such as seen in hypothyroidism—and you take in more calories than you burn, the body then establishes a new, higher weight set point.

For example, take the example of a woman who weighs 160 pounds at 5’7” who maintains her weight on 2500 calories a day. She becomes hypothyroid and over the period of a year or two gains 50 pounds. Technically, based on body weight alone, she now needs 2800 calories a day to maintain her weight of 210 pounds. If she kept her calorie intake at 2500, would she lose the extra 50 pounds? Rarely, because not only is her hypothyroidism slowing down her metabolism, but as she drops calories and weight her metabolic rate actually slows down as well. So she might lose some weight, but she will have a higher set point, even as she is consuming the same level of calories as another woman who far less.

This issue of metabolism is one of the factors behind the mystery of someone who apparently eats even more than you do, doesn’t exercise more, but maintains a lower weight, or conversely, someone who doesn’t eat as much as you, but doesn't eat that much and gains weight or can’t lose weight.

Changes in Brain Chemistry

Hunger, satiety, fat storage, and fat burning are all intricately tied to your brain chemistry and a number of key hormones and neurotransmitters. There are neurotransmitters that are released to trigger hunger and to encourage you to eat quick sources of energy like simple carbohydrates. Other neurotransmitters tell you you’ve had enough to eat and are satisfied. Hormones direct glucose in your blood to be stored in fat cells, or instruct the body to release stored glucose for energy.

This complex system can be dramatically affected by several factors that are usually seen in hypothyroidism:

  • Thyroid disease can slow down the metabolism. If your appetite does not drop to match a lower metabolism, what your brain perceives as the right level of food intake to satisfy your hunger may be greater than your metabolism and cause weight gain.
  • Thyroid disease and autoimmunity are chronic stressors for the body. Add to that life stress, and other physical stress like insufficient sleep or nutritional deficiencies, and the physical effects of stress appear, including increased cortisol levels and lower serotonin levels. Increased cortisol can make you more tired, and more effective at fat storage, and lower serotonin can reduce your sense of well-being and trigger cravings for carbohydrates and overeating.

Insulin and Leptin Resistance

Insulin is a hormone released by your pancreas. When you eat foods that contain carbohydrates, your body converts the carbohydrates into simple sugars. These sugars enter the blood, becoming glucose, or blood sugar. Your pancreas then releases insulin to stimulate the cells to absorb the glucose and store it as an energy reserve, returning your blood sugar to a normal level.

For an estimated 25 percent of the population (and some experts estimate that this is much higher in people with hypothyroidism) eating a "normal amount" of carbohydrates raises blood sugar to excessive levels. A substantial percentage of the population also eats a diet that is too high in carbohydrates. In both cases, the pancreas increases insulin release to drive down blood sugar. Over time, however, cells can become less responsive to insulin, and more has to be produced to maintain normal blood sugar levels.

Researchers have also shown a link between resistance to leptin—a hormone that helps regulate fat storage and fat burning—and thyroid disease.

Both insulin resistance and leptin resistance have a number of negative effects:

  • They can make you hungry, especially for carbohydrate-rich foods
  • They can lower the amount of sugar your body burns as energy, or prevent your body from effectively releasing and using stored fat
  • They can make your cells even better at storing fat, and even worse at removing fat.
  • They can increase your risk of developing type 2 diabetes.
  • They can cause weight gain, or make weight loss more difficult

The Controversy

The issue of weight gain—or difficulty losing weight—in hypothyroidism is controversial. Many conventional medicine experts believe that there is no direct relationship between thyroid function and obesity. At the same time, numerous research studies have found that the interaction between thyroid hormone, fat tissue, other hormones, and the brain are all crucial for weight control and maintenance of metabolism and energy

Studies have shown that, on average, weight modestly decreases following treatment for hypothyroidism and that thyroid stimulating hormone (TSH) levels are typically higher in people who are overweight or obese, compared to the normal population. Research into thyroid patient quality-of-life consistent shows weight gain or inability to lose weight as a key concern for people with hypothyroidism.

There is, however, more definitive evidence that links autoimmune diseases—especially Hashimoto thyroiditis, the cause of most hypothyroidism in the U.S.—with weight gain and obesity. Some research has shown that in some people, autoimmunity triggers resistance to leptin, which then becomes a major contributor to a higher metabolic set point, and the inability to lose weight.

A Word From Verywell: There Are Solutions

Don’t give up hope. You can successfully lose weight with hypothyroidism by paying attention to resolving the key issues we just described. Specifically:

  • If your TSH level falls in the higher end of the reference range, discuss with your doctor whether a dosage increase and a lower target TSH level might be best for you.
  • Have your free T3 levels checked, and if your free T3 is not in the top half of the reference range, discuss with your doctor whether T3/T4 combination therapy may be best for you.
  • Exercise! Regular exercise—ideally at least 30 minutes five times a week—is crucial, as it can help raise your metabolism, curb your appetite, lower blood glucose levels, lower insulin and leptin resistance, increase your serotonin levels, and lower your cortisol. Just be sure not to do too much high-intensity, exhausting exercise as that can actually be more stressful and raise cortisol levels.
  • Limit your eating window. Leptin resistance is often associated with habits such as frequent snacking or multiple smaller meals per day. Experts on leptin resistance recommend eating only 2 to 3 meals per day, with no between-meal snacks. They also suggest not eating after 8 p.m. and allowing a 12 hour “fasting period” overnight to help sensitize the body to leptin.
  • Consider type 2 diabetes drugs. There is evidence that taking type 2 diabetes drugs such as metformin or injectable drugs, will increase your sensitivity to insulin and may help reduce both insulin and leptin resistance.

Sources:

Garber, J, Cobin, R, Gharib, H, et. al. Clinical Practice Guidelines for Hypothyroidism in Adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocrine Practice. Vol 18 No. 6 November/December 2012.

Duntas LH, Biondi B. The interconnections between obesity, thyroid function, and autoimmunity: the multifold role of leptin. Thyroid. 2013 Jun;23(6):646-53. doi: 10.1089/thy.2011.0499. Epub 2013 Apr 4.

Pearce EN. Thyroid hormone and obesity. Curr Opin Endocrinol Diabetes Obes. 2012 Oct;19(5):408-13. doi: 10.1097/MED.0b013e328355cd6c.

Santini F, et al. Mechanisms in endocrinology: the crosstalk between thyroid gland and adipose tissue: signal integration in health and disease. Eur J Endocrinol. 2014 Oct;171(4):R137-52. doi: 10.1530/EJE-14-0067.

Versini M. et. al. Obesity in autoimmune diseases: not a passive bystander. Autoimmun Rev. 2014 Sep;13(9):981-1000. doi: 10.1016/j.autrev.2014.07.001. Epub 2014 Aug 2.

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