When it comes to Functional Medicine and thyroid disorders, hypothyroidism tends to get all the press. In the United States, hypothyroidism is more common than its counterpart, hyperthyroidism. However, what few people know is hyperthyroidism can be far more dangerous than hypothyroidism. Furthermore, the conventional medical treatments available for hyperthyroidism are harsh and can have lasting adverse health effects. Functional Medicine is uniquely poised to fill the need for safe and effective treatments for hyperthyroidism. Read on to learn what hyperthyroidism is, what causes it, how it is treated in conventional medicine, and how a Functional Medicine approach can improve symptoms and potentially reverse the disease’s course.
Hyperthyroidism, while less common than its more famous counterpart, can be far more dangerous. Check out this article for more about what causes the condition and how it can be treated through a Functional Medicine approach. #functionalmedicine #chriskresser
- 1 A Quick Overview of Thyroid Function
- 2 What Is Hyperthyroidism?
- 3 What Causes Hyperthyroidism?
- 4 How Is Hyperthyroidism Diagnosed?
- 5 Graves’ Disease: Statistics, Signs, Symptoms, and Long-Term Complications
- 6 The Conventional Approach to Hyperthyroidism
- 7 The Functional Medicine Approach to Hyperthyroidism
- 8 The Underlying Causes of Hyperthyroidism
- 9 How to Treat the Root Cause of Your Hyperthyroidism
A Quick Overview of Thyroid Function
To understand how hyperthyroidism impacts the body, it helps to first understand a bit about thyroid physiology. Thyroid function is regulated by the pituitary gland, a tiny gland in your brain that produces and releases thyroid-stimulating hormone (TSH). TSH travels to the thyroid gland, activating the production of thyroxine (T4) and triiodothyronine (T3). T4 is the precursor to T3, the biologically active form of thyroid hormone.
What Is Hyperthyroidism?
Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, causing a dramatic increase in metabolism.
The dramatic upswing in metabolism triggered by hyperthyroidism causes:
- Rapid weight loss
- Tachycardia and irregular heartbeat
- Nervousness and anxiety
- Eye disease
- Menstrual changes
Hyperthyroidism is less common than hypothyroidism. While hypothyroidism affects nearly 5 percent of U.S. adults, just 1 percent experience hyperthyroidism. (1, 2)
Overt versus Subclinical Hyperthyroidism
Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is also referred to as “primary hyperthyroidism.” It is characterized by a low TSH level and elevated T4 and T3. T4 is the prohormone of T3, the most biologically active form of thyroid hormone. Graves’ disease is the most common form of overt hyperthyroidism. However, a subset of patients with hyperthyroidism has high T4 and normal T3; this condition is referred to as “T4 toxicosis.” T4 toxicosis is more common in patients with inflammatory diseases, as the chronic inflammation reduces the conversion of T4 to T3, resulting in “normal” T3 levels despite the presence of thyroid hyperactivity. T4 toxicosis is seen in up to 10 percent of elderly patients with hyperthyroidism. (3)
Subclinical hyperthyroidism occurs when TSH is low but T3 and T4 are normal. Subclinical hyperthyroidism is defined as having a “low but detectable” TSH of 0.1 to 0.4 mIU/L. (4) The introduction of more sensitive assays for assessing serum TSH concentrations over the past few decades has led to a surge in the diagnosis of subclinical hyperthyroid cases. (5)
What Causes Hyperthyroidism?
From a purely diagnostic standpoint, there are four leading causes of hyperthyroidism:
- Graves’ disease
- Toxic adenoma
- Toxic multinodular goiter
Graves’ disease, as I mentioned above, is the most common cause of overt hyperthyroidism. It accounts for approximately 60 to 80 percent of all cases of hyperthyroidism. (6) It is an autoimmune disease that results in stimulating thyroid growth and thyroid hormone release.
Hashitoxicosis is a transient form of hyperthyroidism in individuals with Hashimoto’s disease, an autoimmune disorder that causes hypothyroidism. The transient hyperthyroidism is triggered by inflammation that disrupts the thyroid follicular cells, where T4 and T3 are made, resulting in an excess release of thyroid hormone. Hashitoxicosis usually lasts for one to two months, after which the thyroid reverts back to a hypothyroid state. (7)
Toxic adenoma and toxic multinodular goiter are two other causes of hyperthyroidism that involve a strong genetic component. Toxic adenoma occurs when a single nodule on the thyroid gland causes increased thyroid hormone production. Multinodular goiter consists of the growth of independently functioning nodules in the thyroid gland that stimulates the production of T3 and T4 without TSH. These conditions are more common in developing countries where iodine intake is insufficient.
Genome-wide association studies have attempted to identify genetic risk factors for Graves’ disease, the most common cause of overt hyperthyroidism. So far, the overall effect size for genetic markers related to Graves’ disease is weak, suggesting that other non-genetic factors are more likely involved. Epigenetic mechanisms, which are significantly impacted by diet and lifestyle, are more likely to influence the course of Graves’ disease. (8, 9)
How Is Hyperthyroidism Diagnosed?
Several modalities are used to diagnose hyperthyroidism. Blood testing to assess thyroid hormones and thyroid antibodies is the first step. Suppressed TSH with high free T4 or free T3 or both confirm a diagnosis of overt hyperthyroidism. However, TSH can appear low and free T4 and T3 can appear normal in subclinical hyperthyroidism. Measurement of TSH receptor antibodies has a sensitivity of 97 percent and a specificity of 99 percent for the diagnosis of Graves’ disease. (10)
A radioactive iodine uptake test is the next step. This test involves administering a small dose of radioactive iodine; the goal is to determine how much iodine the thyroid gland takes up. A high iodine uptake is indicative of hyperthyroidism.
Ultrasound may also be used to look at the thyroid; it is useful for detecting nodules on the thyroid that may be producing an excess of thyroid hormone.
Graves’ Disease: Statistics, Signs, Symptoms, and Long-Term Complications
Graves’ disease is by far the most common form of overt hyperthyroidism in the United States. It affects around one in 200 people (though subclinical Graves’ disease could be more prevalent) and is several times more common in women than men. (11, 12, 13) While women are more commonly affected, men tend to be more severely affected by the disease. The age of onset of Graves’ disease is typically between the ages of 20 and 40.
Graves’ disease is caused by the production of TSH receptor antibodies, also known as thyroid-stimulating immunoglobulins (TSIs). TSI activates the TSH receptor, replicating TSH’s action and stimulating the production of T3 and T4 by the thyroid gland. However, Graves’ disease is also accompanied by a lack of negative feedback inhibition. This causes excessive production of thyroid hormone by the thyroid gland, with no control point for inhibiting further thyroid hormone production.
Graves’ disease is a condition rife with anomalies. For example, up to 25 percent of Graves’ disease cases spontaneously remit, for unknown reasons. (14) Furthermore, many patients with Graves’ disease spontaneously become hypothyroid; an even higher percentage of patients with Graves’ disease, approximately 80 percent, who undergo radioactive thyroid treatment eventually become hypothyroid. (15)
TSI activity triggers an array of unique signs and symptoms characteristic of Graves’ disease. TSI stimulates cells in the eyes, causing a condition of bulging eyes referred to as Graves’ ophthalmopathy. TSI also stimulates skin (dermal) cells and may cause a condition called pretibial myxedema, localized lesions of the skin caused by the deposition of hyaluronic acid in the skin. Other symptoms of Graves’ disease include:
- Anxiety and nervousness
- Hair and nail changes
- Weight loss, including reductions in both lean mass and fat mass (interestingly, up to 10 percent of patients with Graves’ disease experience weight gain instead) (16)
- Increased heart rate
- Increased systolic blood pressure
- Heat intolerance
- Sexual dysfunction
- Increased body temperature
- Frequent bowel movements
- Nausea and vomiting
- Muscle weakness
- Swollen lymph nodes
- Increased appetite
Conditions Associated with Graves’ Disease and Long-Term Complications
Graves’ disease is associated with a range of other conditions that are primarily autoimmune in nature. It is linked to:
- Pernicious anemia
- Type 1 diabetes
- Myasthenia gravis
- Rheumatoid arthritis
- Addison’s disease
- Celiac disease
Left untreated, Graves’ disease can cause serious health complications, including cardiovascular issues like left ventricular hypertrophy and heart failure, excessive bone resorption and loss of bone density, myopathy, infertility, and pregnancy complications. (17, 18, 19, 20, 21) If T3 is too high, it can trigger a thyroid storm, heart attack, stroke, and even death. The risks and complications of hyperthyroidism are more severe than with Hashimoto’s disease and hypothyroidism.
The Conventional Approach to Hyperthyroidism
Unfortunately, the conventional medicine approach to hyperthyroidism leaves much to be desired. Treatment options include suppressing thyroid function through medications, destroying the thyroid gland through radiation, or removing the thyroid altogether in a procedure known as “total thyroidectomy.”
While thyroid-suppressive medications certainly have a time and place in the management of hyperthyroidism, radioactive thyroid treatment and thyroidectomy are drastic procedures with long-term severe health outcomes. Furthermore, none of these treatments address the underlying causes of hyperthyroidism.
Several medications are used in the conventional medical management of hyperthyroidism. When TSH is low, and thyroid hormones are high, methimazole and propylthiouracil (PTU) are typically used. These drugs are thyroperoxidase (also known as thyroid peroxidase, or TPO) inhibitors, meaning they inhibit an enzyme called TPO, which adds iodine atoms onto tyrosine residues, an essential step in producing T4 and T3. TPO inhibitors, thus, make it harder for the thyroid gland to produce thyroid hormone. PTU also reduces the peripheral conversion of T4 to T3 in extrathyroidal tissues.
While TPO inhibitors can help prevent acute complications of hyperthyroidism, such as the “thyroid storm,” a rare, life-threatening condition that can occur in untreated or undertreated hyperthyroidism, they may not be ideal interventions over the long-term. Complications of methimazole and PTU treatment include:
- Gastrointestinal upset
- Joint pain
- Paresthesia—a numb or tingling feeling in the extremities
- Hair loss
Less frequent but more severe complications include agranulocytosis (a sharp reduction in the number of white blood cells in the blood), aplastic anemia (the failure to produce sufficient red blood cells), and liver and kidney inflammation. (22) However, PTU may be safer than methimazole for the treatment of Graves’ disease during pregnancy. (23)
Other medications that are often prescribed to patients with hyperthyroidism include beta-blockers to reduce the anxiety and abnormal heart rhythms that occur with hyperactive thyroid function. Calcium channel blockers may also be used to reduce a rapid heart rate.
Radioactive ablation of the thyroid gland is another treatment option offered in conventional medicine for Graves’ disease. This procedure permanently destroys the thyroid gland’s ability to make thyroid hormones. Radioactive iodine is used for this procedure because iodine has a high affinity for the thyroid gland; the radioactive isotope of iodine travels to the thyroid gland, where the radioactivity destroys the cells in the thyroid gland, reducing thyroid hormone output.
Potential complications of radioactive iodine treatment include worsening Graves’ ophthalmopathy and the development of radiation thyroiditis, which causes an exacerbation or recurrence of Graves’ disease in 15 to 20 percent of patients. (24)
Unfortunately, radioactive iodine doesn’t just affect the thyroid gland; many other organs and tissues also have an affinity for iodine and may inadvertently take up some radioactive iodine in circulation. For example, the ovaries have a high affinity for iodine. Research suggests that women undergoing radioactive iodine treatment for Graves’ disease can have normal pregnancy outcomes if they stop treatment for at least six months pre-conception and if their thyroid function is well-maintained throughout pregnancy. (25) While this sounds encouraging, we are still in the early days of understanding how radioactive iodine treatment may influence fertility and pregnancy, fetal, and infant health outcomes.
Finally, surgical removal of the thyroid gland is another option offered for hyperthyroidism by conventional medicine. Subtotal thyroidectomy involves removing a portion of the thyroid gland, preserving a degree of thyroid function. Ideally, this approach should negate lifelong thyroid hormone replacement therapy. Unfortunately, many individuals who undergo subtotal thyroidectomy go on to develop hypothyroidism and must be treated with exogenous thyroid hormone anyway. There is also a small but significant risk of persistent hyperthyroidism post-surgery. An observational study of patients with Graves’ disease who underwent subtotal thyroidectomy for their disease found that a mere 6 percent developed normal thyroid function post-surgery; 84 percent developed hypothyroidism, and 10 percent had persistent or recurrent hyperthyroidism. (26) Based on these pretty abysmal findings, the researchers ultimately agreed that “subtotal thyroidectomy seems to provide very little advantage over total thyroidectomy in terms of postoperative thyroid function.”
Total thyroidectomy, on the other hand, removes the entire thyroid gland. Thyroidectomy risks include damage to the recurrent pharyngeal nerves, which are the nerves connected to the vocal cords, causing hoarseness. Damage to the parathyroid glands, which regulate calcium levels, and difficulty swallowing may also occur post-surgery. The risks of these complications are not small, either; one study indicates that hypocalcemia may occur in nearly 54 percent of people who undergo total thyroidectomy. (27)
The Functional Medicine Approach to Hyperthyroidism
The Functional Medicine approach to hyperthyroidism differs from the conventional approach. It seeks to address the underlying causes of hyperthyroidism, rather than suppress symptoms or obliterate thyroid function. While treatment with thyroid-suppressive medications can help manage an acute hyperthyroid crisis, it is not the only treatment option.
The first step in the Functional Medicine approach to hyperthyroidism is to take an in-depth look at thyroid function markers. You’ll want to look at your TSH, total T4, total T3, free T4, and free T3. You’ll also want to ask your doctor to check for TPO and thyroglobulin antibodies and TSI/TSH receptor antibodies. While not essential, you could also look at reverse T3, the free T4 index, and T3 uptake.
These markers are similar to those that you would assess for hypothyroidism, with the only difference being that you’ll also look at TSI/TSH receptor antibodies. When assessing hyperthyroidism, the lower end of the conventional and optimal ranges is essentially the same; it’s the upper ends of these ranges that differ.
Functional Ranges for Thyroid Hormones and Antibodies
The functional ranges for thyroid hormones and antibodies are:
- TSH functional range: 0.5–2.0 mU/L
- Total T4 functional range: 6.0–12 ug/dL
- Total T3 functional range: 100–180 ng/dL
- Free T4 functional range: 1.0–1.5 ng/dL
- Free T3 functional range: 2.5–4.0 pg/mL
- TPO antibodies reference range: 0–34 IU/mL
- Thyroglobulin antibodies reference range: 0.0–0.9 IU/mL
- TSH receptor antibodies (TSI) reference range: 0–139 IU/mL
Ancillary markers that can also support hyperthyroidism diagnosis include aspartate aminotransferase (AST) and alanine aminotransferase (ALT); some studies suggest that these markers are elevated in Graves’ disease. Urine iodine (24-hour, spot) or hair iodine measurement may also be useful for ruling out iodine supplementation as a potential cause of Graves’ disease.
Functional Medicine is a medical model, distinct from the conventional approach, that promotes true wellness and healing for patients. It’s focused on addressing the root cause of illness, and it offers practitioners a way to prevent or even reverse chronic diseases like hyperthyroidism. If you’re a licensed practitioner looking for a better way to help your patients, the Functional Medicine approach could be the methodology you’ve been searching for. Find out how you can integrate Functional Medicine into your practice with the ADAPT Practitioner Training Program.
The Underlying Causes of Hyperthyroidism
Functional Medicine seeks to understand the underlying causes of hyperthyroidism. It directs treatment toward resolving those factors, rather than merely suppressing thyroid function or ablating it completely.
A growing body of research indicates that the gut microbiome plays a critical role in the development and progression of Graves’ disease. Patients with Graves’ disease also demonstrate lower gut microbial diversity, a higher abundance of Prevotella and Haemophilus parainfluenzae, and a lower abundance of Alistipes and Faecalibacterium. Gut microbes may influence the progression of autoimmune hyperthyroidism through several mechanisms:
- People with Graves’ disease demonstrate a lower abundance of gut bacteria involved in T-regulatory cell production, which helps prevent thyroid autoimmunity. (28)
- In rat studies, gut bacteria have been shown to regulate intestinal iodine uptake, thyroid hormone degradation, and the enterohepatic recirculation of thyroid hormone, thus contributing to increased or decreased thyroid hormone levels in the body. (29) A similar process is likely to occur in humans.
- Patients with Graves’ disease demonstrate high levels of antibodies against the gut pathogens Yersinia enterocolitica and Helicobacter pylori, suggesting that chronic gut infections and ensuing immune dysregulation may contribute to the pathogenesis of hyperthyroidism. (30)
Together, these findings suggest that gut dysbiosis may be a critical junction in the development of autoimmune hyperthyroidism.
A substantial body of research indicates a critical link between gluten intolerance and autoimmune disease, including autoimmune thyroid diseases.
A study of 280 people with Graves’ disease and 120 people with Hashimoto’s disease found that 5.5 percent were positive for anti-gliadin antibodies (AGA). This was a statistically significant finding, and further research is certainly warranted given that AGA is but one marker for gluten sensitivity. (31) Patients with Graves’ disease also demonstrate high anti-glutamic acid decarboxylase antibodies, which point toward gluten sensitivity. (32) Researchers note that celiac disease and autoimmune thyroid diseases share common immunological mechanisms. (33)
Gliadin, the protein portion of gluten, may trigger Graves’ disease due to its structural similarity to thyroid tissue. When the intestinal barrier is compromised (due to factors such as gut dysbiosis and antibiotic use), gliadin escapes the gut and enters the bloodstream. In the systemic circulation, the immune system tags gliadin as a threat, marking it for destruction; however, in the process, it can also inadvertently “tag” thyroid tissue, targeting it for destruction, as well.
Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysfunction
The pituitary gland and thyroid gland work together to regulate thyroid hormone production. HPA axis dysfunction may, thus, interfere with thyroid function and influence the development of hyperthyroidism. (34) Chronic stress is a potent trigger for HPA axis dysfunction, so managing stress may be necessary for resolving hyperthyroidism.
Several chronic infections are linked to Graves’ disease. As I mentioned above in our discussion of gut health, H. pylori and Y. enterocolitica infections are linked to Graves’ disease. However, extraintestinal infections, such as Epstein-Barr virus and hepatitis C virus, may also play a role. (35, 36) These pathogens produce proteins that share structural similarities with the TSH receptor. The immune system may be thrown off by these similarities, causing it to launch an attack against both the pathogen and thyroid tissue.
A growing body of research indicates that anthropogenic pollutants, or toxins released by human activities such as industry and agriculture, interfere with thyroid function. Exposure to mercury may disrupt thyroid function by interfering with deiodinases, which activate and deactivate thyroid hormones. (37) Common sources of mercury exposure include fish and shellfish, dental amalgams, and airborne mercury vapor from industry.
Sufficient iodine is essential for healthy thyroid function; however, too little or too much can push the thyroid into hypothyroidism or hyperthyroidism. This is why trying to achieve the recommended daily intake of iodine (150 mcg/day) primarily from food, which offers physiologically appropriate iodine levels, may be safer than supplements.
Vitamin D and selenium are also essential for normal thyroid function. Observational research links low vitamin D with the onset of Graves’ disease; vitamin D is a potent immunomodulator. Low levels of the nutrient may predispose individuals to immune dysregulation and, subsequently, thyroid autoimmunity. (38)
Selenium is an essential cofactor for several antioxidant enzymes involved in healthy thyroid function. Low selenium may increase the risk of thyroid autoimmunity, including Graves’ disease, by reducing antioxidant protection mechanisms in the thyroid gland, increasing the thyroid gland’s susceptibility to oxidative stress. (39)
Insulin Resistance and Blood Sugar Dysregulation
The increase in metabolism triggered by hyperthyroidism leads to an elevated demand for glucose by body tissues, increasing endogenous glucose production through glycogen breakdown in muscles and gluconeogenesis in the liver. (40) In some people with hyperthyroidism, the disposal of excess glucose is impaired by the presence of insulin resistance, a phenomenon in which the body’s cells do not respond well to the hormone insulin and can’t easily take up glucose from the blood. The mechanisms linking insulin resistance and hyperthyroidism have not been fully explained, but may be related to higher circulating levels of inflammatory signaling molecules in hyperthyroidism, which impair insulin sensitivity. (41)
Diet and lifestyle changes can significantly improve insulin sensitivity, offering adjunct support in the Functional Medicine treatment of hyperthyroidism.
Immune System Shifts Post-Pregnancy
In women, it is not uncommon for autoimmune thyroid conditions to appear after pregnancy. Pregnancy increases T-regulatory cell activity, which allows the mother’s body to maintain “tolerance” to the baby growing inside of her. However, after pregnancy, this natural immune-suppressive state is lost, and the immune system may skew in the opposite direction, triggering a loss of self-tolerance and the production of autoantibodies to one’s own tissues, including the thyroid gland. This explains why some women experience the onset of autoimmune thyroid diseases, including both Hashimoto’s and Graves’ disease, in the postpartum period. (42)
How to Treat the Root Cause of Your Hyperthyroidism
Functional Medicine seeks to resolve the underlying issues that contribute to hyperthyroidism. The Functional Medicine approach to hyperthyroidism includes diet and lifestyle changes, smart supplementation, and the judicious use of specific medications, namely low-dose naltrexone (LDN).
Diet and Nutrition
Gluten avoidance is a must for individuals with hyperthyroidism, given the profound interactions between gluten, the immune system, and thyroid function. (43) However, a gluten-free diet alone may be insufficient to correct the gut dysbiosis, chronic inflammation, and nutrient deficiencies associated with hyperthyroidism; this is where a Paleo template diet comes in. A Paleo template diet removes common dietary triggers of inflammation, such as acellular carbohydrates and industrial seed oils, and can, thus, help reduce inflammation that may contribute to sleep disruption. You can learn more about the Paleo template in my article “Beyond Paleo: Moving from a ‘Paleo Diet’ to a ‘Paleo Template’.”
For some people with Graves’ disease, the autoimmune protocol (AIP) may be superior even to the Paleo template for alleviating symptoms, at least in the short-term. The AIP diet removes additional dietary triggers that can provoke inflammation, including eggs, nightshades, nuts, and seeds. Clinical research has found the AIP diet useful for alleviating Hashimoto’s thyroiditis; these benefits may carry over into autoimmune hyperthyroidism, as well. (44)
Antioxidant Vitamins C and E
Whether you choose to follow a Paleo template or AIP diet, you must consume sufficient micronutrients that support healthy thyroid function. Antioxidant nutrients, such as vitamins C and E, are essential for attenuating the excess oxidative stress in Graves’ disease. (45, 46) Vitamin C is found in:
- Red bell pepper
- Brussels sprouts
- Citrus fruits
Vitamin E is found in:
- Extra virgin olive oil
- Nuts and seeds
Iodine is essential for healthy thyroid function and is found primarily in sea vegetables such as dulse and wakame and seafood. Individual tolerance of iodine varies from one person to the next, so finding the right dietary intake level to support your thyroid may necessitate some experimentation. While high doses of iodine may be temporarily beneficial for people with Graves’ disease due to the inhibitory effects of high-dose iodine on thyroid hormone synthesis, this process should be overseen by a qualified endocrinologist with experience in this area.
The thyroid gland contains the highest selenium level per milligram of tissue in the body, indicating a high organ-specific need for this nutrient. (47) Selenium is a cofactor for glutathione peroxidase, an enzyme that may protect the thyroid gland from oxidative damage, and for iodothyronine deiodinase, an enzyme important for the activation and deactivation of thyroid hormones. (48, 49) Selenium supplementation has been shown to attenuate Graves’ ophthalmopathy, possibly by enhancing the portion of the immune system that produces T-regulatory cells. (50)
You can find selenium in a variety of foods. Brazil nuts are by far the most selenium-rich food, providing 554 mcg of selenium per serving. However, selenium is also found in:
- Sunflower seeds
Research indicates that vitamin D deficiency is common in people with Graves’ disease, and supplementation may have a protective effect against Graves’ disease recurrence. (51, 52) Sun exposure is the best source of vitamin D, but you can also find it in cod liver oil, pastured egg yolks, and fatty cold-water fish. In situations where one’s vitamin D level is low, supplementation can be beneficial.
Zinc, Vitamin A, and Magnesium
The roles of zinc, vitamin A, and magnesium in hyperthyroidism are less well understood than the roles of iodine, selenium, and vitamin D. However, preliminary research suggests that abnormal metabolism of zinc, vitamin A, and magnesium may occur as a result of hyperthyroidism. Zinc and vitamin A are crucial elements of cell signaling pathways that regulate immune function, while magnesium is required for over 300 different enzymatic pathways in the body. (53, 54) Repletion of these nutrients in patients with hyperthyroidism may support healthier immune function and whole-body well-being.
A variety of nutraceuticals are employed in the Functional Medicine approach to hyperthyroidism. Curcumin, the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and glutathione offer anti-inflammatory and antioxidant properties that may help counteract the excess oxidative stress associated with hyperthyroidism. (55, 56) Probiotics support gut health while prebiotics feed beneficial gut bacteria, improving the health of the gut milieu.
L-carnitine is an amino acid analog that, at high doses of 2 to 4 grams per day, inhibits the entry of T4 and T3 into the cell nucleus, reducing the effects of hyperthyroidism. (57) The most bioavailable form of L-carnitine is acetyl-L-carnitine. Botanicals such as bugleweed and lemon balm have long been used in traditional herbalism to balance hyperactive thyroid function and may be useful adjunct treatments alongside other dietary and lifestyle changes.
While Functional Medicine tends to not be as heavy-handed with pharmaceuticals as conventional medicine, there is undoubtedly a time and place for medications in the functional approach to hyperthyroidism. LDN is one medication that can be very helpful, with minimal to no side effects, in the treatment of hyperthyroidism.
LDN modulates opioid receptors throughout the body, increasing the release of endorphins with immune-modulating effects. (58) LDN is particularly helpful for attenuating autoimmune responses. To learn more about LDN, check out my article “Low-Dose Naltrexone: A Promising Drug for Hard-to-Treat Conditions.”
Last but certainly not least, lifestyle modifications are essential elements of recovery from hyperthyroidism. Managing stress with a daily stress-reduction practice, such as meditation, getting plenty of high-quality sleep, and regularly moving your body, supports healthy immune function and a balanced inflammatory response, prerequisites for creating an unshakeable foundation for healing and long-term thyroid health.
A diagnosis of hyperthyroidism doesn’t need to lead to a lifelong reliance on medication, invasive surgery, or destruction of thyroid function altogether. With a Functional Medicine approach, it is possible to not only alleviate symptoms of hyperthyroidism but to reverse the underlying conditions that lead to it in the first place.