Low Dose Naltrexone (LDN)
Low‑dose naltrexone (LDN) is a low dose of naltrexone that is thought to briefly block opioid receptors to boost natural endorphins and support immune balance.
Graves’ disease is an autoimmune disease and the most common cause of hyperthyroidism. Diffuse immune stimulation causes thyroid overactivity, resulting in excess thyroid hormone, triiodothyronine (T3) and thyroxine (T4). When thyroid hormone is too high, otherwise known as thyrotoxicosis, the body transitions into a hypermetabolic state. Due to its autoimmune root cause, Graves’ disease patients tend to experience clinical features like graves ophthalmology disease (thyroid eye disease) and goiter as well as typical hyperthyroid symptoms, like heart palpitations and fatigue.
Graves’ disease medication is designed to control the hyperthyroidism or limit the thyroid inflammation. Remission is the goal after extended therapy because antithyroid drugs for Graves disease can reduce the production of thyroid hormones, but are not a permanent cure. Low dose naltrexone (LDN) is an immune modulator and an anti-inflammatory agent, and can serve as supportive therapy to address the underlying autoimmunity. Some patients choose to permanently alter their thyroid tissue via surgery, often resulting in hypothyroidism.
Compounded Medications for Graves’ Disease
What is Graves’ Disease?
Causes
As with many autoimmune disorders, Graves’ disease causes are unclear, though genetics and environment can both be factors. If a parent has Graves’ Disease, genetic predisposition can put an individual at a higher susceptibility of inheriting the condition. This increased risk does not dictate how autoimmunity will present and impact daily life.
Graves’ disease is an autoimmune disease that results in hyperthyroidism, a state of thyroid hormone excess. Not all hyperthyroidism is caused by Graves’ disease. In this condition, the immune system produces autoantibodies that malfunction by constantly activating the thyroid stimulating hormone (TSH) receptor. TSH is a hormone released by the pituitary gland that tells the thyroid how much and when to release thyroxine (T4) and triiodothyronine (T3). When the body targets its own TSH receptor via autoantibodies, excess thyroid hormone is produced and the thyroid gland grows, presenting as a diffuse goiter. Because Graves’ disease causes are rooted in autoimmunity, other autoimmune problems typically arise throughout the body as well.
Symptoms
Graves’ disease symptoms are two-fold: there is a hyperthyroid element and an autoimmune element. The autoimmune piece of the disease can lead to additional unique problems, as effects can be localized or spread throughout the body.
Graves’ ophthalmopathy, also known as thyroid eye disease, is specific to this condition and can persist or worsen even when thyroid hormone levels normalize. It occurs when autoantibodies attach to TSH receptors on orbital fibroblasts, causing increased orbital pressure. The inflammation can lead to lid retraction, eye bulging and swelling of the eye socket.
Graves’ dermopathy (pretibial myxedema), is relatively rare and generally exclusive to the disorder. It looks like thickened, hyperpigmented skin nodules on patients’ shins that resemble an orange peel.
The excessive antibody activation of the TSH receptor can cause increased cell growth and blood flow to the thyroid gland. What may result is a diffuse, symmetrical goiter located at the front of the neck.
Autoimmune diseases like Graves’ can have fluctuating symptoms as the condition waxes and wanes. The severity of these symptoms of Graves disease may ebb and flow as autoimmunity progresses over time. Patients can swing from hyperthyroid to euthyroid – some may experience transient hypothyroidism. Autoimmunity of any kind can show up in different ways in different people.
Graves’ disease causes hyperthyroidism, and those symptoms are a reflection of a hypermetabolic state, where the body can eventually depletes itself. This hypermetabolic state can have negative consequences resulting in symptoms like heart palpitations, weight loss, anxiety, insomnia, and excessive sweating and/or heat intolerance.
Therapies
Graves’ disease medications address complications from an overactive thyroid, and low dose naltrexone (LDN) can support the autoimmune component of the disorder. While there is no cure for thyroid disease, medication or a surgical procedure like a thyroidectomy could be necessary to prevent long-term complications from overstimulation of the heart and nervous system.
Antithyroid drugs for Graves’ disease like methimazole block thyroid peroxidase, the enzyme responsible for helping generate T3 and T4. This drug is considered first-line therapy. Similarly, propylthiouracil (PTU) stops thyroid hormone synthesis and prevents the conversion of T4 into T3, the more active hormone form. However, this medication is less preferred due to its increased risk of liver toxicity. In some cases, 12 to 18 months of therapy can help patients achieve remission.
As a complement to antithyroid drugs for Graves’ disease, low dose naltrexone (LDN) can be prescribed as supportive therapy. Low dose naltrexone (LDN) is a Graves’ disease medication that targets the underlying autoimmunity that drives the disorder. By modulating the immune system and impacting inflammation, LDN can improve quality of life and potentially benefit patients that struggle with fluctuating disease severity or relapses. LDN is considered adjunctive therapy, as it cannot address hyperthyroidism directly.
Beta-blockers like propranolol can help control certain hyperthyroidism symptoms quickly, such as heart palpitations and tremors, but they do not address the root cause of the thyroid problem.
Commonly Asked Questions About Grave’s Disease
Graves’ disease is an autoimmune disease that results in hyperthyroidism, a state of thyroid hormone excess. Not all hyperthyroidism is caused by Graves’ disease. In this condition, the immune system produces autoantibodies that malfunction by constantly activating the thyroid stimulating hormone (TSH) receptor. When the body targets its own TSH receptor via autoantibodies, the thyroid gland grows and excess thyroid hormone is produced.
Medical professionals like endocrinologists or thyroidologists receive specialized training to clinically support patients with Graves’ disease. General practitioners like primary care physicians are important for routine monitoring and functional medicine providers offer a holistic approach to autoimmune disease management. If surgery is required, an ENT (ear, nose, and throat) surgeon is an appropriate fit.
Graves’ disease is an autoimmune form of hyperthyroidism that may go into remission, but there is no cure for autoimmunity. Remission means the autoimmune overstimulation of the thyroid has decreased enough that thyroid hormone production has normalized. The other determining factor is maintaining this state without requiring medication for 12 months or more. Other causes of hyperthyroidism may resolve depending on the cause.
