Thank you! Your submission has been received!
Oops! Something went wrong while submitting the form.
Subscribe to the Magazine for free
Subscribe for free to keep reading! If you are already subscribed, enter your email address to log back in.
Thanks for subscribing!
Oops! Something went wrong while submitting the form.
Are you a healthcare practitioner?
Thanks for subscribing!
Oops! Something went wrong while submitting the form.

Subclinical Hypothyroidism: Signs, Symptoms, & Treatments

Medically reviewed by 
Subclinical Hypothyroidism: Signs, Symptoms, & Treatments

Subclinical hypothyroidism (SCH) doesn't meet the diagnostic criteria for overt hypothyroidism, but it is a mild and early form of underactive thyroid dysfunction commonly caught in functional medicine practices.  

In up to 10% of the general population, SCH can develop into clinical hypothyroidism. One study found that 26.8% of those with SCH progressed to hypothyroidism within six years of their diagnosis. Treating SCH has been long debated, as the literature on the benefits of treatment continues to produce mixed results. Utilizing a functional medicine approach for diagnosis and treatment can optimize thyroid function and prevent progression to overt hypothyroidism, regardless of whether conventional therapy is brought on board. (1)


What is Subclinical Hypothyroidism

The thyroid is an endocrine gland located in the neck that is responsible for synthesizing and releasing thyroid hormones into the body. Thyroid hormones act on every tissue in the body so that they can use energy and keep the body's organs functioning optimally. (2)

SCH is a mild precursor of hypothyroidism in which lab work reveals an elevated thyroid stimulating hormone (TSH) level with normal thyroid hormone, T4, and T3 levels. Because T4 and T3 are not low, this condition does not meet guidelines for overt hypothyroidism, a condition in which the thyroid under-produces thyroid hormones but does have the potential to progress into it.

How Thyroid Hormones Communicate With Each Other

The hypothalamic-pituitary-thyroid (HPT) axis ensures that normal thyroid hormone levels exist within the circulation. (2, 3, 4)

  • The thyroid gland synthesizes and secretes into the bloodstream two hormones: thyroxine (T4) and triiodothyronine (T3).
  • T4 is the predominant hormone made by the thyroid gland, and in circulation, it is converted to its biologically active counterpart, T3, which acts on cell receptors to exert its effects.
  • In normal scenarios, a small percentage of T4 is also converted into reverse T3 (rT3), a largely inactive form of thyroid hormone that the body cannot use. In cases of high stress or trauma, T4 conversion may begin to favor the rT3 pathway, creating an imbalance in the T3-to-rT3 ratio.
  • The brain constantly monitors thyroid hormone levels in circulation. When it detects low circulating thyroid hormone levels, the hypothalamus secretes the thyrotropin-releasing hormone (TRH).
  • TRH acts on the brain's pituitary gland to signal the secretion of thyroid-stimulating hormone (TSH).
  • TSH travels to the thyroid gland and stimulates the synthesis and release of thyroid hormones into the circulation.
  • Thyroid hormones exert negative feedback onto the brain to slow the production of TRH and TSH, preventing the overproduction of thyroid hormones.

Why is It Important to Look At Optimal Thyroid Lab Values

Conventional thyroid guidelines recommend that TSH be the only test ordered for thyroid dysfunction screening (6). It is estimated that screening with TSH alone will miss 7% of individuals with hypothyroidism. A narrower, more optimal, standard reference range for TSH has been proposed, given that individuals with thyroid dysfunction were included in setting the current reference range for a healthy thyroid.

Analyzing thyroid lab values with optimal reference ranges ensures that individualized medicine is practiced and that cases of thyroid dysfunction are addressed.  

Functional medicine providers will typically begin assessing thyroid health by ordering a comprehensive thyroid panel, including many other thyroid markers (discussed in more detail below). This supports a thorough understanding of how the HPT axis is functioning and what may be contributing to thyroid dysfunction if it is present.

Optimal Thyroid Lab Values

Subclinical Hypothyroidism Signs & Symptoms

Most subclinical hypothyroidism cases present without symptoms, especially when TSH is only mildly elevated. When symptoms do arise, they are usually vague and mild. Symptoms may include:

  • Fatigue
  • Brain fog
  • Unexplained weight gain
  • Constipation
  • Depression
  • Inability to tolerate cold temperatures
  • Changes to menstrual periods
  • Dry skin
  • Hair loss

Elevations in triglycerides, total cholesterol, and LDL-cholesterol are common in patients with hypothyroidism. Less severe and less consistent findings of dyslipidemia (changes in blood lipid levels) can present on blood cholesterol panels in patients with SCH. (5)

What Causes Subclinical Hypothyroidism  

SCH and hypothyroidism share the same causes.

Globally, iodine deficiency is the most common cause of hypothyroidism. However, this is uncommon in the United States and other iodine-replete areas.

Autoimmune thyroid disease, known as Hashimoto's thyroiditis, is the most common cause of hypothyroidism in the United States. This is secondary to the formation of antithyroid antibodies that attack the thyroid, create an inflammatory state within the thyroid gland, and impair thyroid function.

Other causes of hypothyroidism include (5):

  • Medication-induced: commonly prescribed medications include lithium and amiodarone
  • Injury to the thyroid gland, such as during surgery on the head or neck
  • Treatments for hyperthyroidism: radioactive iodine therapy, antithyroid medications, and partial removal of the thyroid gland

Some may be at increased risk for developing SCH. Risk factors include:

  • Gender: For reasons that remain unclear, women are more likely to develop SCH than men.
  • Age: Older adults are more likely to have higher levels of TSH and thyroid dysfunction.
  • Iodine Intake: Both excess and deficient iodine intake can increase the risk of developing thyroid disease.
  • Genetics: You are at higher risk of having Hashimoto's-related SCH if you have a family member with a thyroid disorder or other autoimmune disease.

Functional Medicine Labs to Request For Thyroid Health

Comprehensive Thyroid Panel

In patients who have been screened for thyroid dysfunction with only TSH, and whose results have returned elevated, conventional guidelines recommend that TSH be repeated with a free T4 measurement within two weeks to three months to confirm a diagnosis of SCH. Patients without symptoms but with TSH levels between 4.5-10.0 mIU/L should have TSH remeasured at a minimum every six to 12 months. Your doctor may recommend more frequent repeat thyroid testing to monitor changes in thyroid function, especially if changes to the treatment plan have been implemented.

A comprehensive thyroid panel commonly includes these thyroid markers:

  • TSH
  • Free T4
  • Free T3
  • Reverse T3
  • Anti-Thyroglobulin (Anti-TG) Antibody
  • Anti-Thyroid Peroxidase (Anti-TPO) Antibody

Ordering a comprehensive thyroid panel can reduce repeat confirmatory testing, giving insight into how the HPT axis is functioning, how the thyroid synthesizes hormones, and how effectively those hormones are being converted.

Positive thyroid antibodies confirm a diagnosis of thyroid autoimmunity, which increases the risk of SCH progressing to clinical hypothyroidism.

Micronutrient Panel

A micronutrient panel is a blood test that helps to establish how the gut absorbs nutrients from the diet and how those nutrients are absorbed and utilized by the cells that need them. Thyroid-specific nutrients required for synthesizing and converting thyroid hormones include tyrosine, iodine, selenium, magnesium, iron, zinc, B vitamins, and vitamins A, E, and D.

Comprehensive Stool Test

There is accumulating data that a strong thyroid–gut axis exists, and identifying and treating gut conditions can improve thyroid health (7-11).

Dysbiosis is a common finding in thyroid disorders as it alters the immune response by promoting inflammation and reducing immune tolerance, damaging the intestinal membrane and causing an increase in intestinal permeability. Dysbiosis can directly impact thyroid hormone levels through its deiodinase activity and the inhibition of TSH. Gut microbiota also influences the absorption of essential minerals to the thyroid.

A comprehensive stool analysis is an advanced stool test that measures biomarkers related to digestive function, intestinal inflammation, and the gut microbiome. Balancing the gut microbiome has been correlated with reducing inflammatory markers, thyroid antibodies, and TSH levels (10).

Functional Medicine Treatment for Subclinical Hypothyroidism

The indications for conventional treatment of subclinical hypothyroidism with levothyroxine, and thyroid hormone replacement, have not definitively been established due to insufficient evidence to support pharmaceutical intervention. As of now, it is generally recommended that a watch-and-wait approach be taken for those with TSH levels under 10mIU/L and without symptoms to prevent overtreatment and thyrotoxicosis, a state of excess circulating levels of thyroid hormone.

A shared decision-making approach should be implemented between doctor and patient, and the decision to administer levothyroxine should consider the extent of thyroid dysfunction, comorbid conditions, risk factors, and patient preference.

Utilizing a functional approach to treatment, however, provides alternative therapeutic options that address the root cause of thyroid dysfunction. Based on lab results a practitioner can make an individualized approach to the patients treatment plan.


There is not one established best "hypothyroidism diet." Eating a balanced diet rich in whole fruits and vegetables, dietary fiber, healthy fats, and lean protein supports an anti-inflammatory environment in the body and is one of the best nutritional approaches to supporting thyroid function and mediating thyroid symptoms.

Identifying and removing food triggers can be helpful for some thyroid patients. The most researched food sensitivity correlated with autoimmune hypothyroidism is gluten, especially in those with concurrent Celiac disease. Existing research shows reduced thyroid autoimmunity and improved response to thyroid medication after initiating a gluten-free diet.

If a patient is on a thyroid replacement medication, some foods can impair the absorption of the drug, rendering it less effective. It is recommended to take the thyroid medication at least an hour before or after eating, drinking, or taking other medications/supplements to avoid interactions.  

Herbs & Supplements

The thyroid-gut axis speaks to the notion that intestinal health influences thyroid health and vice versa. In some cases, addressing gut health may improve thyroid conditions. Based on the micronutrient and comprehensive stool test, a practitioner can make an individualized approach to the patient's specific needs for digestive and thyroid support.

Probiotics: can be an excellent place to start in improving gut health if your comprehensive stool or micronutrient results suggest intestinal dysfunction. Probiotics can improve the balance of microorganisms in the intestines, reduce inflammation, and support intestinal healing.

Vitamin D: Research suggests that vitamin D deficiency is associated with a higher level of thyroid antibodies and that vitamin D supplementation may decrease anti-TG and anti-TPO levels within six months.

Magnesium: is required for T4-to-T3 conversion and iodine uptake into thyroidal cells. Magnesium deficiency is also associated with an increased risk of autoimmunity. Not only can magnesium supplementation support thyroid health, but it can also treat hypothyroid-related constipation by acting as a natural laxative.

Ashwagandha: is classified as an adaptogenic herb that has anti-inflammatory and neuroprotective properties. Ashwagandha is most commonly implemented as a therapy to manage stress, anxiety, and depression and can help manage these hypothyroid-related symptoms. Although limited research exists, this preliminary study suggests that it may improve thyroid hormone levels in hypothyroid patients. It is postulated that this is due to its ability to reduce oxidative stress, which can cause cell and tissue damage in excess.

Ginger root: is a highly anti-inflammatory herb with antioxidant, anti-nausea, antimicrobial, and pain-relieving effects. Ginger can be used in symptom palliation and improving cardiovascular profiles, as research supports that it effectively lowers LDL-cholesterol levels.

Lifestyle changes

Stress changes how our body produces cortisol, our "stress hormone." Not only can imbalanced cortisol impact thyroid function, but it can also exacerbate hypothyroid-like symptoms (14). Incorporating relaxation and mindfulness techniques daily, such as deep breathing, journaling, or meditation, can promote a healthy stress response.

Inadequate sleep over long periods will affect hormone synthesis and rhythms, immune system function, and metabolism, among other critical bodily functions. Not only can poor sleep disrupt thyroid function, but it can also exacerbate hypothyroid symptoms like fatigue and brain fog. Establishing a regular wind-down routine and sleep schedule, aiming for at least eight hours of sleep nightly, will promote healthy sleep quality.


Subclinical hypothyroidism is an early stage of thyroid disease in which thyroid markers display signs of dysfunction within the HPT axis. Many cases will progress to clinical hypothyroidism and pose the potential for increased risk for other health concerns without treatment. Conventional pharmaceutical therapy poses a risk of inappropriately high levels of circulating thyroid hormone, which cannot be ignored. A functional approach to SCH opens doors to safe alternatives for therapy when the conventional model currently outlines a gray treatment zone and limited therapeutic options.

The information provided is not intended to be a substitute for professional medical advice. Always consult with your doctor or other qualified healthcare provider before taking any dietary supplement or making any changes to your diet or exercise routine.
Learn More
No items found.

Lab Tests in This Article

1. Fatourechi, V. (2009). Subclinical Hypothyroidism: An Update for Primary Care Physicians. Mayo Clinic Proceedings, 84(1), 65–71.

2. American Thyroid Association. (2020, June 8). Thyroid Function Tests.

3. Schroeder, A. C., & Privalsky, M. L. (2014). Thyroid Hormones, T3 and T4, in the Brain. Frontiers in Endocrinology, 5.

4. Decesaris, L. (2022, August 8). Treating the Thyroid Naturally. Rupa Health.

5. Adlin, V.E. (1998). Subclinical hypothyroidism: deciding when to treat. American Family Physician, 57(4), 776–780.

6. Sheehan, M. T. (20`). Biochemical Testing of the Thyroid: TSH is the Best and, Oftentimes, Only Test Needed – A Review for Primary Care. Clinical Medicine &Amp; Research, 14(2), 83–92.

7. Centanni, M., Gargano, L., Canettieri, G., et al. (2006). Thyroxine in Goiter,Helicobacter pyloriInfection, and Chronic Gastritis. New England Journal of Medicine, 354(17), 1787–1795.

8. Bugdaci, M. S., Zuhur, S. S., Sokmen, M., et al. (2011). The Role of Helicobacter pylori in Patients with Hypothyroidism in Whom Could Not be Achieved Normal Thyrotropin Levels Despite Treatment with High Doses of Thyroxine. Helicobacter, 16(2), 124–130.

9. Choi, Y. M., Kim, T. Y., Kim, E. Y., et al. (2017). Association between thyroid autoimmunity and Helicobacter pylori infection. The Korean Journal of Internal Medicine, 32(2), 309–313.

10. El-Zawawy, H. T., Farag, H. F., Tolba, M. M., et al. (2020). Improving Hashimoto’s thyroiditis by eradicating Blastocystis hominis: Relation to IL-17. Therapeutic Advances in Endocrinology and Metabolism, 11, 204201882090701.

11. Ruchała, M.,  Szczepanek-Parulska, E., & Zybek, A. (2011). The influence of lactose intolerance and other gastro-intestinal tract disorders on L-thyroxine absorption. Endokrynologia Polska, 63(4), 318–323.

12. Lakhan, S. E., & Kirchgessner, A. (2010). Gut inflammation in chronic fatigue syndrome. Nutrition &Amp; Metabolism, 7(1), 79.

13. Carabotti, M., Scirocco, A., M.A. Maselli, et al. (2015). The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of Gastroenterology, 28(2), 203–209.

14. Shekhar, S., McGlotten, R., Auh, S., et al. (2020). The Hypothalamic-Pituitary-Thyroid Axis in Cushing Syndrome Before and After Curative Surgery. The Journal of Clinical Endocrinology &Amp; Metabolism, 106(3), e1316–e1331.

Subscribe to the Magazine for free to keep reading!
Subscribe for free to keep reading, If you are already subscribed, enter your email address to log back in.
Thanks for subscribing!
Oops! Something went wrong while submitting the form.
Are you a healthcare practitioner?
Thanks for subscribing!
Oops! Something went wrong while submitting the form.