You already know you have hypothyroidism. Your doctor checked your TSH, saw it was high, wrote you a prescription for levothyroxine, and sent you on your way.

But here’s what you probably don’t know:

The real underlying cause of your hypothyroidism.

And for a thyroid patient, this changes everything.

Why?

Because while Hashimoto’s is the #1 cause of hypothyroidism^[1]^[2], it’s a potentially reversible cause (or at least, a very manageable cause)^[3], and knowing you have it changes a lot about your treatment.

Instead of just throwing thyroid medication at your problem and tracking your TSH, you have real tools that may be able to reverse your condition.

Which is why you need to know the 5 signs that indicate your “hypothyroidism” is actually Hashimoto’s in disguise:

#1. Your Symptoms Swing From Hypo To Hyper

Run-of-the-mill hypothyroidism is actually pretty boring.

You feel tired, cold, slow, and you feel that way most of the time.

Hashimoto’s is different:

Because it’s primarily an autoimmune disease that attacks your thyroid gland, your thyroid symptoms can fluctuate, sometimes wildly, day to day.

When your immune system attacks your thyroid gland tissue, it damages your cells. It just so happens that the primary job of these cells is to either store or release your thyroid hormone.

This damage can do one of two things: reduce the amount of thyroid hormone your gland produces or increase it.

When it increases it, you’ll feel swings of hyperthyroidism.

When it decreases it, you’ll feel the exact opposite.

If you feel like you’re on a rollercoaster with your symptoms, this is the reason, and it’s a strong indication that your hypothyroidism is caused by Hashimoto’s.

By the way, this problem has a name; it’s called Hashitoxicosis, and it looks enough like Graves’ disease that a 2026 case series was published on Hashimoto’s patients who were incorrectly diagnosed with Graves’ disease because of it^[4].

#2. Your Labs Swing Up and Down

All thyroid patients will see some swings in their TSH levels as they get repeated tests.

But what you shouldn’t see is large swings of multiple points from test to test. In healthy people, a change of about 0.75 in TSH is enough to count as a real change, and each person’s normal range is only about half as wide as the lab’s^[5].

Here’s what I mean:

If your TSH was 1.2 in March, 5.8 in July, and 2.9 in November and your doctor didn’t change your dose in between, this is a problem.

Normally, your TSH is primarily driven by your thyroid medication dose. And outside of some unique circumstances, your TSH should stay relatively stable as long as your dose of thyroid medication stays the same.

Big changes in TSH levels with a stable dose of thyroid meds points to one thing:

An immune system flare-up that is actively damaging your thyroid gland.

Of course, this damage is a problem by itself, but the swings cause another, perhaps even bigger, problem:

And that’s chasing your TSH.

When your doctor sees a swing in your TSH, he or she will try to make up the difference by either adjusting your dose up or down.

But these changes in thyroid function are always behind because your current TSH is a reflection of what already happened in your body.

As a result, your symptoms continue to swing wildly from hypo to hyper, your dose never feels quite right, and your doctor remains puzzled.

#3. Foods Make Your Symptoms Worse

It may be hard to put your finger on it exactly, but let me ask you a question:

Does your intuition tell you that your body does better on some foods and worse on others?

Does it feel like certain foods trigger inflammation or thickness in your neck or thyroid gland?

If so, this isn’t just your imagination.

There’s a real, solid, physiologic connection between your gut and your thyroid gland^[6], which is especially important if you have Hashimoto’s.

This is for two reasons:

Roughly 70% of your immune system lives in your gut^[7], which means the food that you eat comes into direct contact with it.
Certain compounds (like gluten) look very similar to thyroid tissue to your immune system^[8]. So if they enter your body, it can confuse your immune system.

Celiac disease, for instance, shows up in about 1 in 62 people with autoimmune thyroid disease^[9], and in Hashimoto’s patients without celiac, 6 months gluten-free lowered TSH and raised free T4 in a pooled analysis of four studies^[10].

While it may seem depressing to hear that you may need to give up certain foods if you have Hashimoto’s, there’s some silver lining:

It works in the opposite direction, too. Which means that eating healthy food can have a positive impact on thyroid gland function.

The bottom line? If you feel there is a connection between your diet and your thyroid, think Hashimoto’s.

#4. Your Symptoms Can’t All Be Explained By Your Thyroid

Low thyroid function produces a fairly predictable list of symptoms: fatigue, weight gain, constipation, cold hands and feet, dry skin, hair loss, brain fog, and heavy periods.

Hashimoto’s produces that exact same list, plus some extras:

Joint pain^[11], hives^[12], flu-like symptoms, low-grade fevers (or chills), joint tenderness, unexplained rashes, lymph node sensitivity, and tissue swelling.

The cause of the extras is related to the immune system.

When your immune system is flared up, you’ll start to experience many of the same symptoms you might experience as if you were sick.

This isn’t a true “sickness” or “illness” type of thing, but it’s an easy way to think about it.

These extra symptoms can make finding a diagnosis very difficult, because most doctors aren’t in the habit of connecting them to your thyroid gland, but that’s where these are originating.

The problem with these symptoms is that they aren’t connected to thyroid gland function; they are connected to immune function.

And they can persist even when your thyroid labs look otherwise completely normal^[11].

If your symptoms are fluctuating and you have some extras that are hard to explain, think Hashimoto’s.

#5. Autoimmune Disease Runs In Your Family

Do you have a mother, sister, or daughter with celiac disease, vitiligo, psoriasis, rheumatoid arthritis, type 1 diabetes, or lupus?

This single question does more diagnostic work than you’d think, and it takes only a few seconds to answer.

Hashimoto’s has a strong genetic component, and twin studies put its heritability at roughly 65%^[13].

The largest family study ever done on it looked at 92,405 Hashimoto’s patients and nearly 3 million of their relatives in the Utah Population Database.

First-degree relatives had 1.77 times the odds of developing it, second-degree relatives 1.23 times, and third-degree relatives 1.11 times.

Spouses also had higher odds, which tells you the environment you share matters too, not only the genes.

Autoimmune diseases also cluster within the same person.

A cross-sectional study of 1,053 newly diagnosed Hashimoto’s patients found that a second autoimmune disease was common and that it became more common with age^[14].

Practically, this means if you are someone with an existing autoimmune disease like celiac disease or vitiligo and you start to experience hypothyroid-like symptoms, there’s a very high chance Hashimoto’s is the cause.

When asking about family history, these are the ones you want to look for because they are the ones associated with Hashimoto’s:

Celiac disease, autoimmune gastritis, type 1 diabetes, rheumatoid arthritis, Sjogren’s syndrome, lupus, vitiligo, alopecia areata, and Addison’s disease.

How To Find Out For Sure: The 2 Tests To Ask For

Nothing we’ve discussed will prove that you have Hashimoto’s (it just gives you a very good idea), but there are two tests that you can order:

TPO antibodies (thyroid peroxidase antibodies) and thyroglobulin antibodies (sometimes written as TgAb or anti-TG).

The next time you go to your doctor, ask them to order both.

Believe it or not, most doctors aren’t in the habit of ordering these tests automatically because, in their mind, whether or not you have Hashimoto’s doesn’t change their treatment for you.

But the reality is quite the opposite: having this information changes everything for you.

Here’s how to interpret your results:

First, a positive result means you have Hashimoto’s. There’s no real ambiguity here and no second opinion necessary.

The presence of these antibodies against your own tissues is never a normal finding^[15].

Second, the quantity of your result is important.

A TPO level of 900 doesn’t mean you’re 9 times sicker compared to someone with a TPO level of 90, but it does give you some useful information.

For instance, you can use your antibody levels to determine whether or not a given treatment is working.

You can usually assume that if your antibody levels are decreasing with whatever treatment you are using, that this is a good thing (this isn’t always true, but it is more often than it is not)^[16]^[17].

Unfortunately, you may be met with some resistance when asking to get these tests from your doctor.

If that happens, you can order both yourself through almost any direct-to-consumer lab in the country, without a physician’s signature.

If there’s one thing to take away from this information, it’s this:

If you have hypothyroidism and you live in the United States, there’s about a 75-90% chance your condition is caused by Hashimoto’s.

And if that’s the case, there’s something you can do about it.

If you aren’t sure where to start, try my Hashimoto’s supplement quiz.

It will walk you through your symptoms and provide you with a list of supplements tailored to your specific situation.

It’s 100% free, and you can access it here.

Scientific References

1. Kaur, J., et al. (2026). Hashimoto Thyroiditis. StatPearls.

2. Chaker, L., et al. (2017). Hypothyroidism. The Lancet. doi:10.1016/S0140-6736(17)30703-1.

3. Ragusa, F., et al. (2019). Hashimotos’ thyroiditis: Epidemiology, pathogenesis, clinic and therapy. Best Practice & Research Clinical Endocrinology & Metabolism. doi:10.1016/j.beem.2019.101367.

4. Akl, M.M., et al. (2026). Clinical Case Series of Destructive Thyrotoxicosis Associated with Hashimoto’s Thyroiditis Misdiagnosed as Graves’ Disease: Clinical Patterns, Diagnostic Pitfalls, and Hypothesized Molecular Insights. Problemy Endokrinologii. doi:10.14341/probl13651.

5. Andersen, S., et al. (2002). Narrow individual variations in serum T4 and T3 in normal subjects: a clue to the understanding of subclinical thyroid disease. The Journal of Clinical Endocrinology & Metabolism. doi:10.1210/jcem.87.3.8165.

6. Cayres, L.C.F., et al. (2021). Detection of Alterations in the Gut Microbiota and Intestinal Permeability in Patients With Hashimoto Thyroiditis. Frontiers in Immunology. doi:10.3389/fimmu.2021.579140.

7. Vighi, G., et al. (2008). Allergy and the gastrointestinal system. Clinical & Experimental Immunology. doi:10.1111/j.1365-2249.2008.03713.x.

8. Fan, X., et al. (2026). Beyond celiac disease: the potential role of gluten in Hashimoto’s thyroiditis. Frontiers in Endocrinology. doi:10.3389/fendo.2026.1811207.

9. Roy, A., et al. (2016). Prevalence of Celiac Disease in Patients with Autoimmune Thyroid Disease: A Meta-Analysis. Thyroid. doi:10.1089/thy.2016.0108.

10. Piticchio, T., et al. (2023). Effect of gluten-free diet on autoimmune thyroiditis progression in patients with no symptoms or histology of celiac disease: a meta-analysis. Frontiers in Endocrinology. doi:10.3389/fendo.2023.1200372.

11. Punzi, L., et al. (2002). Clinical manifestations and outcome of polyarthralgia associated with chronic lymphocytic thyroiditis. Seminars in Arthritis and Rheumatism. doi:10.1053/sarh.2002.33722.

12. Tienforti, D., et al. (2022). Chronic urticaria and thyroid autoimmunity: a meta-analysis of case-control studies. Journal of Endocrinological Investigation. doi:10.1007/s40618-022-01761-2.

13. Bujnis, M., et al. (2025). Familial Risk of Hashimoto’s Thyroiditis in a Large Genealogical Database. The Journal of Clinical Endocrinology & Metabolism. doi:10.1210/clinem/dgaf251.

14. Ruggeri, R.M., et al. (2017). Autoimmune comorbidities in Hashimoto’s thyroiditis: different patterns of association in adulthood and childhood/adolescence. European Journal of Endocrinology. doi:10.1530/EJE-16-0737.

15. Hollowell, J.G., et al. (2002). Serum TSH, T4, and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). The Journal of Clinical Endocrinology & Metabolism. doi:10.1210/jcem.87.2.8182.