An Update on Thyroglobulin Antibodies

Clinical Take Home Points

Functional Medicine “Bias”

• It is common to see functional medicine providers test for thyroglobulin antibodies. Occasionally, we’ve seen this marker used to diagnose patients with Hashimoto’s who have otherwise normal thyroid function tests. 

Study Purpose

• What’s the clinical utility and significance (if any) of thyroglobulin antibodies?

What Does The Evidence Suggest?

• TgAb have a notable prevalence in the general population and have poor sensitivity/specificity for diagnosing Hashimoto’s.
• Overall, TgAb levels have little utility in diagnosing Hashimoto’s when compared to TPOAb. They may be able to help identify the 10-20% of Hashimoto patients with negative TPOAb in the presence of painless goiter or hypoechogenicity on thyroid ultrasound. 
• TgAb may be helpful in tracking thyroid cancer prognosis and women at risk for postpartum thyroiditis. 
• Debate surrounds the prognostic value of TgAbs and thus, TPOAb levels are a better prognostic marker. 

What Should I Do In Clinical Practice?

Thyroglobulin antibodies in the healthy population

• High-Level Overview
  • Tg antibodies may be detected in up to ¼ of the general healthy population

• Supporting Research 
  • “Tg antibodies (Tg Abs) are polyclonal antibodies to Tg. Tg Abs are common in autoimmune thyroid disease, with a prevalence of 20%–90% in Hashimoto thyroiditis and 30%–60% in Graves’ Disease, but, like TPO Abs, they are also present in 10%–27% of healthy adults” [1]
  • The NHANES analysis of 17,000 participants found TgAb positivity in 10.4% of the healthy population.

Are thyroglobulin antibodies useful for diagnosing Hashimoto’s?

• High-Level Overview
  • TgAbs have poor sensitivity/specificity for diagnosing Hashimoto’s. However, they may be helpful to distinguish the 10-20% TPO-negative individuals with Hashimoto’s.

• Supporting Research
  • Tg antibodies may be more of a sign than a cause of thyroid tissue destruction.
    • “The production of antibodies against Tg can be induced by massive destruction of the thyroid gland, but high Tg levels in blood do not per se induce antibody production” [2]
  • TPOAbs are more sensitive and specific. TgAbs do NOT correlate well with TPOAb.
    • “Antibodies to thyroglobulin, the most abundant protein of the thyroid gland, are less sensitive (positive in only 60–80% of HT patients) and less specific (positive in a greater proportion of healthy controls) than thyroperoxidase antibodies. Nevertheless, they have their own utility. Although they are requested together with TPOAbs by ingrained clinical practices and fluctuate in parallel after therapeutic interventions, the two thyroid antibodies correlate poorly” [3]
  • TgAbs are NOT specific for Hashimoto’s thyroiditis and may be found in other autoimmune disorders.  They have a low sensitivity of 30-50%.
    • “On the contrary, a positive antibody is not diagnostic of Hashimoto’s thyroiditis because Tg antibodies are found in numerous other conditions. They are present in approximately 50% of Graves’ disease cases, 20% of non-toxic goiter and thyroid cancer cases, and also in normal individuals, especially older females. Tg antibodies are also found in non-thyroid autoimmune diseases, such as Sjögren’s syndrome, myasthenia gravis, celiac disease, and type 1 diabetes” [4]
    • “AbTg are present in circulation in 60-80% of patients with autoimmune thyroid disease (AITD), and 40-60% of patients with Graves’ Disease. The determination of circulating AbTg has a sensitivity of 30-50% for the diagnosis of AITD.” [5]
    • “Both TgAbs and TPOAbs are detected when the patient is suspected to have autoimmune hypothyroidism. However, TgAb alone in the absence of TPOAb is not significantly associated with thyroid disease. In addition, TPOAb are more prevalent than TgAb in GD. The sensitivity and specificity of TgAbs are not as good as those of TPOAbs in the diagnosis and prognosis of AITDs. All of these factors may weaken the necessity of the measurement for TgAbs since the test for TPOAbs alone seems enough” [6]
  • However, Tg antibodies may be helpful to distinguish the 10-20% TPO-negative individuals with Hashimoto’s.
    • “TG autoantibodies frequently accompany those against TPO, but occur less frequently in isolation, which has led to suggestions that there is no place for measuring TG autoantibodies for the diagnosis of AITD. In other series, however, TG autoantibodies measured by ELISA, in the absence of TPO autoantibodies, have been reported in around 20% of patients with AITD and were associated with larger thyroid volume, small nodular formation in the gland, and less frequent hypothyroidism, than in patients with both TG and TPO autoantibodies. These differences depend largely on the methods of analysis, and it is likely that measurement of TG autoantibodies by sensitive assays (radioimmunoassay in particular) will indeed detect some patients with AITD who are negative for TPO autoantibodies” [7]

Other utility of thyroglobulin antibodies?

• High-Level Overview
  • Positive thyroglobulin antibodies may indicate a higher likelihood of:
    • Postpartum thyroiditis 
    • Thyroid cancer

• Supporting Research 
  • TgAbs may indicate a higher likelihood of postpartum thyroiditis.
  • This study found that the addition of TgAb increased the risk of postpartum thyroiditis.
    • 296 pregnant women, classified into 4 groups according to thyroid antibody status in first trimester:
      • 97 women: TPOAb+/TgAb-
      • 35 women: TPOAb-/TgAb+
      • 85 women: TPOAb+/TgAb+
      • 79 women: TPOAb-/TgAb-
    • Followed thyroid status x2-3 years postpartum.
    • Overall, 19.9% developed postpartum thyroiditis.
    • TPOAb (OR 2.3) and TgAb (OR 3.1) had a higher rate of postpartum thyroiditis:
      • 6.3% TPOAb-/TgAb-
      • 16.5% TPOAb+/TgAb-
      • 22.9% TPOAb-/TgAb+
      • 35.3% TPOAb+/TgAb+
    • TgAb positivity was not associated with poor maternal or fetal adverse outcomes.
  • Positive thyroglobulin antibodies may indicate a worse prognosis for thyroid cancer. 
    • Thyroid cancer patients have a 2.5x higher rate of TgAb than healthy controls (25% vs 10%) [8].
    • “It is now well accepted that Tg can be used to monitor metastases in well-differentiated thyroid carcinoma. However, a difficulty in monitoring serum TgAb levels in this situation is the relatively high prevalence of TgAb in the population, even in some euthyroid individuals. Interference by these TgAb may lead to overestimation or underestimation of the Tg concentration, depending on the assay used. On the other hand, there is growing evidence that TgAb can be used as a surrogate for Tg.” [9] See image below and note how both TgAb and TPOAb decrease after thyroid cancer treatment.
      
      
    • In a retrospective study of 1,600 patients with thyroid nodules, TgAb positivity was higher in those who developed thyroid cancer (31% vs 20%, OR 1.6).
    • Another study found a 2.1 times higher likelihood of development of thyroid cancer in patients who had nodules and a TgAb >40 IU/mL. This association was independent of TSH, TPOAbs, and other confounding factors.

Prognostic value of thyroglobulin antibody levels

• High-Level Overview
  • Limited research has shown that TgAb has overall poor prognostic value.

• Supporting Research 
  • TgAb titers may correlate with total symptom burden.
    • In a study of 290 Hashimoto patients not on thyroid replacement, TgAb was associated with severity and number of symptoms such as fragile hair, edema, and voice hoarseness [10]. This finding was independent of TPOAb, T3, TSH levels and thyroid volume. 
  • TgAb titers do NOT usually correlate with the degree of thyroid dysfunction.
    • The NHANES analysis of 16,500 participants found no significant association between TgAb titer and current TSH/thyroid function. 
      • “TgAb alone in the absence of TPOAb is not significantly associated with thyroid disease.”
  • Results are mixed on whether higher TgAb levels indicate a higher likelihood of future hypothyroidism.
    • This retrospective study of 109 kids with subclinical hypothyroidism found that TgAb titers were associated with a higher risk of requiring levothyroxine in the future (OR 28.2).
    • However, another paper states, “as demonstrated by a prospective study, TgAb, unlike TPOAb, cannot be used to predict the switch from subclinical hypothyroidism to overt hypothyroidism.” [11]

How This Changes Clinical Practice

• Clinical Takeaways
  • TgAb levels have a notable prevalence in the general population and are not specific to Hashimoto’s thyroiditis. 
  • TgAb levels have poor prognostic value for autoimmune thyroid disease for most individuals.
  • However, TgAb may be helpful for assessing the risk of postpartum thyroiditis and thyroid cancer prognosis.
  • TPOAbs are a much better marker for autoimmune thyroid disease. 
  • If you suspect autoimmune thyroid disease and TPOAbs are normal, consider TgAb levels and/or thyroid ultrasound.

• Final Thoughts
  • As compared to TPOAbs, TgAbs has limited research in showing its utility. Given its low sensitivity/specificity, we do not use it in clinical practice. Seeing that up to ¼ of the healthy population has TgAbs, we fear that utilizing this test may lead to unwarranted fear when not used correctly. Until more research has been performed, TgAb levels have limited diagnostic and prognostic value.

• More Resources
  • Our thyroid algorithm
  • Cheat sheet download:
    
    

Mold illness as the cause of non-responsive fibromyalgia symptoms

Patient Summary:

• Overview Context: 
  • Mary is a 56 yo post-menopausal female with good outlook and diet who presents w/ multiple concerns of migraines, chronic fatigue, and functional GI disturbances on polypharmacy regimen to manage symptoms

Visit 1 (Day 1) – History and Exam:

Symptoms and Concerns

• Chief Complaints:
  • Abdominal discomfort & bloating – main concerns
  • Widespread joint pain
  • Fatigue
  • Migraines
  • Insomnia

• Other Symptoms:
  • Multiple chemical sensitivities
  • Lightheadedness
  • Brain fog

• Onset, Timeline and History:
  • 16 years old: put on hormone treatment to start her menstrual cycle. The headaches/migraines started then.
  • Ovary or fallopian tube infection at 17 yo (1981) which led to multiple rounds of antibiotics, surgery & complications. Weight dropped to 85 lbs and developed GI symptoms after infection.
  • Experienced sexual abuse
  • 21 yo: sister died, really hard for her
  • 26 yo: car accident
  • 33 yo: complications for child birth, emergency surgery
  • 41 yo: sterilization secondary to menstrual cycle 3 weeks per month
  • 56 yo: another car accident

Past Medical History

• Prior Diagnosis:  
  • Fibromyalgia
  • Chronic regional pain syndrome
  • Chronic sinusitis

• Medications:
  • Wellbutrin, Depression
  • Lyrica, Fibromyalgia
  • Oxycodone HCI, Cervical Spondylosis
  • Oxycontin, Cervical Spondylosis
  • Albuterol, Mild asthma /allergies
  • Tolterodine, Urinary control
  • Zofran, Nausea
  • Diclofenac topical 1%, alternative to lidocaine
  • Lidocaine topical 2.5%, pain

• Prior Surgical History 
  • Multiple laparoscopic and gynecological surgeries

Prior Testing and Treatment History

• Prior Testing Summary:
  • None

• Previous Diets:
  • None

• Previous Treatments:
  • Helpful
    • Miralax
  • No change
    • Probiotic – just 1 category
    • Ketamine infusions
    • Spinal injections

Initial Impression

• Clinical Questions and Commentary:
  • I highly suspect that some of her chronic pain and migraines are being driven by poor gut health.  Her long-term use of opiates, NSAIDs, and other medications may have disrupted her gut ecosystem. 
  • She also flags for limbic imbalance given her traumatic history, polypharmacy regimen, and my assessment in our first visit
  • I also flagged mold illness given her clinical picture (GI s/sxs, chronic pain, migraines, chemical sensitivities) and will address this if she does not respond to foundational GI therapies

• Differential Dx
  • Poor sleep hygiene, timing, or duration (bed by 2-3 am)
  • Limbic imbalance (rape, sexual abuse, car wreck, death of sister, reactive to loud sounds)
  • SIBO
  • Dysbiosis
  • Hypothyroid
  • Autoimmune Phenomena (vague diagnosis of fibromyalgia)
  • Sleep disordered breathing (snoring, mouth breather, headache)
  • Abdominal/pelvic adhesions (multiple abdominal surgeries)
  • MCAS (symptoms right after eating) 
  • Mold exposure/illness (current home exposure?, spasms)
  • Head trauma/whiplash injury (timing of symptoms)

• Prognosis:
  • Good – Should be mostly GI case but may need to pivot to mold/MCAS if non-responsive. Her case may be more difficult given how many meds she is on 

Visit 2 (1 Week Later) – Testing and Initial Treatment Recommendations

• Recommended Testing
  • Comprehensive blood chemistry panel
  • Autoimmune marker panel (Avise CTD)

• Initial Treatment Recommendations
  • Pull from Plan – Treatment Initial Follow-Up Note
  • Diet:
    • Begin 2-4 day elemental diet reset, followed by optional hybrid approach
    • Other meals should follow low FODMAP
  • Lifestyle:
    • Sleep routine, push bedtime 30-60 minutes earlier
  • Followup:  6-7 weeks

• Clinician Summary
  • First, we will start with foundational GI therapies since that aligns with her main complaints. I also anticipate an improvement in pain/fatigue levels. 
  • I saw this patient around a time I was experimenting with a comprehensive autoimmune panel (Avise CTD). As you will see later, this added little to her care and not something I am performing much anymore.

Visit 3 (8 Weeks Later) - Lab Interpretation and Treatment Evaluation

• Subjective Assessment 
  • Current Symptoms:
    • Improved: 
      • Bloating (20% better)
      • Abdominal discomfort (20% better)
      • Pain (10% better)
      • Fatigue (10% better)
      • Sleep
    • Same: 
      • Migraines
    • Worse: 
      • None
  • Treatment Response:
    • Sleep hygiene – in bed earlier (12:30), better energy
    • Elemental reset to hybrid– did 2.5 days reset, had mild painful defecation, but bloating/abd discomfort better
    • Low FODMAP – helpful for GI symptoms and fatigue

• Lab Results
  • AVISE panel – No antibodies present
  • High MPV w/ low-normal platelets (140), Low B12 (232) 
  • Fasting glucose 92, A1C 5.3%
  • Ferritin 44
  • CRP 1.5
  • Vit D 71
  • TSH 3.7, fT4 1.1, TPOAbs <28
  • tTG-IgA and total IgA normal, deaminated gliadin IgA normal

• Lab Interpretation and Diagnosis
  • No signs of Celiac disease, low iron, anemia, or autoimmune phenomenon
  • Euthyroid without antibodies
  • Low B12 could be from gastritis (or SIBO?)
  • Updated Differential Diagnosis
    • Hypothyroid 
    • Celiac Disease
    • Autoimmune phenomenon
    • Gastritis (GI sxs, low B12, fatigue)
    • Nutritional deficiency (B12 232)

• Impression:
  • Responding well to initial GI therapies. Will continue our work through the GI hierarchy. 
  • As you can see here, the comprehensive autoimmune panel offered little to inform further treatment
  • I’ll get more labs to rule in/out autoimmune gastritis

• Updated Treatment Recommendations
  • New Treatment:
    • Discontinue vitamin D until winter
    • GI: triple probiotic therapy (1 at a time)
    • GI: gut rebuild nutrients
    • NRT: B12 lozenge
  • Testing: intrinsic factor antibodies, anti-parietal cell antibodies
  • Followup: 5-6 weeks

Visit 4 (6 Weeks Later)

• Subjective Assessment 
  • Current Symptoms:
    • Improved: 
      • Bloating (40% better)
      • Abdominal discomfort (40% better)
    • Same: 
      • Fatigue/pain
  • Treatment Response:
    • S. boulardii – may have caused slight constipation
  • Notes:
    • Fibro pain and fatigue had regressed but now has improved the last few weeks

• Lab Results
  • Intrinsic factor antibodies normal
  • Antiparietal cell antibodies normal

• Lab Interpretation and Diagnosis
  • No signs of autoimmune gastritis

• Impression:
  • Getting more improvement with additional GI therapies but pain/fatigue non-responsive. Will discontinue S. boulardii and push further into probiotics and start herbal antimicrobial protocol.

• Updated Treatment Recommendations
  • New Treatment:
    • Core herbal antimicrobial protocol
    • Discontinue S. boulardii
    • Experiment w/ higher end dose range of Lacto/Biff and soil-based probiotic
  • Followup: 4-5 weeks

Visit 5 (5 Weeks Later)

• Subjective Assessment 
  • Current Symptoms:
    • Improved:
      • Bloating (near-resolution)
      • Abdominal discomfort (near-resolution)
      • Lightheadedness
    • Worse: 
      • Pain/fatigue
  • Treatment Response:
    • Electrolytes (self-prescribed) – improved lightheadedness/dizziness
  • Notes:
    • Today, seems to be overly anxious about her symptoms and health

• Impression:
  • Antimicrobials seem to be really helping GI symptoms. Will continue on this for a 2nd month. 
  • May have limbic imbalance that needs attention.

• Updated Treatment Recommendations
  • New Treatment:
    • Continue onto month 2 of herbal antimicrobials
  • Followup: 6-7 weeks

Visit 6 (6 Weeks Later)

• Subjective Assessment 
  • Current Symptoms:
    • Improved:
      • Bloating (resolution)
      • Abdominal discomfort (resolution)
      • Sleep
    • Worse: 
      • Pain/fatigue
  • Treatment Response:
    • On last month of herbal antimicrobials and tolerating well
  • Notes:
    • Attributes fibro flare to new medication from another provider

• Impression:
  • Will give her some more time to establish ‘new baseline’ after finishing herbal antimicrobials but pain/fatigue mostly non-responsive to most GI work. 
  • First, start limbic then transition to MCAS and/or mold as needed.

• Updated Treatment Recommendations
  • New Treatment:
    • Start limbic retraining
  • Followup: 8 weeks

Visit 7 (6 Weeks Later)

• Subjective Assessment 
  • Current Symptoms:
    • Same:
      • Brain fog
      • Headache
      • Fatigue
      • Pain
  • Treatment Response:
    • Had not started on limbic retraining yet
    • Reports being “much happier with gut health” though
  • Notes:
    • Got sick recently and placed on course of antibiotics for vaginal and sinus infections 
    • Most systemic symptoms starting after after she eats

• Impression:
  • Needs to start on MCAS protocol and limbic retraining given sensitivity

• Updated Treatment Recommendations
  • New Treatment:
    • Start limbic retraining
    • MCAS protocol – start 1 at a time every few days
      • Famotidine 20mg (OTC generic form Pepcid AC) – 1 tablet daily, increase to 1 tablet twice daily.
      • Quercetin 500 : 1 capsule 15 minute prior to meals, increase to 2 prior to meals
      • AllQlear – 1 tablet 15 minutes prior to meals, may increase to 2 prior to meals
      • Histamine Block (DAO enzyme): 1 capsule prior to meals, may increase to 2 prior to meals
      • Cetirizine 10mg (OTC generic form of Zyrtec) – 1 tablet daily, increase to 1 tablet twice daily.
  • Followup: 6-8 weeks

Visit 8 (7 Weeks Later)

• Subjective Assessment 
  • Current Symptoms:
    • Same:
      • Brain fog
      • Headache
      • Fatigue
      • Pain
    • Worse:
      • Bloating
      • Abdominal discomfort
  • Treatment Response:
    • DAO enzyme and quercetin – abdominal discomfort, reaction
  • Notes:
    • Reconfirmed past mold exposure and possible current exposure to mold
    • Still has not started limbic retraining

• Impression:
  • Suspicious for mold illness given fatigue/pain/neurological symptoms non-responsive to GI therapies

• Updated Treatment Recommendations
  • New Treatment:
    • Discontinue MCAS protocol
    • Mold empirical binders: 
      • Chlorella
      • Clay
      • Charcoal
  • Testing: RTL Mycotoxin test
  • Followup: 6-8 weeks

Lab Interpretation – No Followup Visit Yet

• Lab Results
  • Ochratoxin – not present
  • Aflatoxin – not present
  • Trichothecene – 0.137 (present)
  • Gliotoxin – 0.863 (equivocal)
  • Zearalenone – 0.568 (equivocal)

• Lab Interpretation and Diagnosis
  • Mold illness likely

• Impression:
  • Labs confirm suspicions of mold illness
  • At next visit, will adjust binders and consider antifungals

Take Home Points

• Highlighted Clinical Rules 
  • Address underlying GI dysfunction before beginning testing or treatment for environmental toxicity including mycotoxicity, heavy metal toxicity as well as chronic infections.
    • All 3 categories of probiotics have shown benefit in reducing mycotoxicity and should be encouraged even in the presence of mold/candida colonization.

• Clinician Commentary
  • It would be tempting to start with mold therapy right out of the gate, but we may have missed the potential of more foundational therapies such as probiotics to first treat the gut and establish a baseline to ensure optimal detoxification. 
  • This is a great example of how chronic pain/fatigue/neuromuscular symptoms that are non-responsive to other diet/lifestyle/GI therapies may be traced back to mold illness as the underlying etiology. 
  • I would really like her to start limbic retraining but this can be a therapy that can be challenging to get patients to do. I ‘sell’ it as something that can lead to benefits with just 10 minutes a day. 
  • Next, I will consider increasing the dose of binders (if previously tolerated), and adding in nasal antifungals +/- systemic antifungals.

Functional Medicine Gone Wrong: A faulty diagnosis of hypothyroidism led to unnecessary medication

Patient Summary:

• Overview Context: 
  • 47 yo female with multiple questionable past diagnoses who is concerned with mostly GI symptoms and multiple sensitivities.

Symptoms and Concerns

• Chief Complaints:
  • Constipation
    • Fluctuating constipation & diarrhea
  • Upper abdominal pain and burning
  • Gas 
    • Associated with constipation 
  • Bloating 
  • Brain fog
  • Headaches
  • Fatigue 
    • “Have low energy every day”
  • Joint pain 
  • Sinus congestion 
  • Hair loss

• Other Symptoms:
  • Palpitations
  • Mood imbalance

• Onset, Timeline and History:
  • 2002 diagnosed with celiac disease and started losing hair
  • 2008 diagnosed with hypothyroidism
  • 2016 Epstein Barr virus after a stressful time
  • 2017 digestive issues started with some gas which resulted in cholecystectomy
  • “Symptoms seemed to explode after this” 
    • Diagnosed with gastritis, exocrine pancreatic insufficiency, acid reflux, hydrogen sulfide SIBO, H. Pylori
    • Treated for these conditions but still having symptoms
  • Many foods, supplements and medications make her feel worse and exacerbate symptoms. 
  • A few months ago, she began experiencing yellow, greasy stools

Past Medical History

• Prior Diagnosis:  
  • Celiac Disease 2002 – Endoscopy confirmed
  • Hypothyroidism 2008
    • Diagnosed by holistic doctor with no blood work – first Armour → NatureThroid→ WP thyroid→ compounded desiccated
    • Historically has had low TSH on thyroid meds
  • EPI 2019 – confirmed by conventional GI, after cholecystectomy
  • Epstein Barr 2016
  • SIBO 2020
  • H Pylori 2020 – FM doc
  • Gastritis 2019 – Endoscopy confirmed
  • Lyme Disease 2022 – FM doc

• Medications:
  • Creon
  • Compounded Desiccated Thyroid replacement
  • Low dose naltrexone
  • Famotidine

• Prior Surgical History 
  • Gallbladder removed, uterine fibroid removed 

Prior Testing and Treatment History

• Prior Testing Summary:
  • Blood testing:
    • tTG IgA <2, total IgA high, deaminated gliadin IgA / IgG wnl, endomysial Ab wnl (on gluten free diet)
    • TSH 1.3, fT4 wnl, No TPO Ab – taking desiccated QOD
  • Stool testing:
    • Elastase <15
    • Calprotectin <16
    • Dysbiosis
    • No parasites

• Previous Diets:
  • Helpful
    • Gluten-Free
    • Dairy-Free
    • Low Histamine
    • Fasting or intermittent fasting
    • Low FODMAP 
  • Reactive
    • High fat diet

• Previous Treatments:
  • Helpful
    • Digestive repair nutrients (glutamine, aloe, etc.)
    • Magnesium
    • Immunoglobulins
    • Bismuth
    • Undecylenic acid
    • Reduce thyroid dose – felt better overall
    • Creon

What Went Wrong?

• Impression:
  • It is very likely that this patient was:
    • 1) Incorrectly diagnosed with hypothyroidism 
    • 2) Put on unnecessary thyroid replacement 
  • She has a glaringly obvious set of GI symptoms that are most likely that cause of her other systemic symptoms
  • An inappropriate hypothyroid diagnosis is evidenced by:
    • No initial blood work for thyroid function
    • No TPO Abs
    • Feeling better off of thyroid meds
    • Multiple switches of thyroid meds with no change in symptoms

• A Better Approach:
  • Treat diet, lifestyle, and gut health before thyroid imbalances in most cases, especially in presence of multiple digestive symptoms.
  • Check history of initial hypothyroidism diagnosis to confirm possible inappropriate thyroid diagnosis.

• Supporting Research:
  • Gut imbalances are 15 times more common than hypothyroidism
    • IBS affects 15% of the population and functional GI disorders affect up to 40% [12, 13, 14]
    • Frank hypothyroidism only affects 1% of the population [15]
  • 34-61% of patients on thyroid replacement may not need their medication
    • A 2020 SR and MA of 17 observational studies involving 1100 patients looked at the effects of discontinuing thyroid hormone replacement. At the median 5 year follow-up, 34.1% had maintained normal thyroid levels. 
    • Another study of 291 patients with questionable diagnosis of hypothyroidism discontinued levothyroxine. After 6-8 weeks, 60.8% had normal thyroid function levels and no adverse effects. 
  • A vast majority of subclinical hypothyroid cases correct on their own with no treatment
    • In a study of 225 subclinical hypothyroid patients, 74% became euthyroid at a 6-month followup without any intervention.