Ferritin, Vitamin B12, and Hashimoto’s: The Hidden Connections Behind Persistent Symptoms

Diana H. Szucs, PharmD

Abstract image of pill-shaped objects

Fatigue, hair loss, brain fog, weakness, feeling cold, and difficulty exercising are commonly blamed on hypothyroidism.

But they are not uniquely thyroid symptoms.

Iron deficiency and vitamin B12 deficiency can cause many of the same problems. This is one reason ferritin and B12 come up so often in discussions about Hashimoto’s — especially when someone continues to feel unwell even after their thyroid hormone levels are under control.

There is a real scientific connection. But it is often oversimplified into claims like:

“Low ferritin causes Hashimoto’s.”

“Hashimoto’s makes you B12 deficient.”

“Everyone with Hashimoto’s should get their ferritin above 70.”

The evidence does not support these statements as written.

At EXPIN, we often think about exposures and biological factors in terms of drivers and triggers. A driver (more subtle, sometimes longer term) is a factor that may contribute to the biological conditions that make disease more likely to develop or persist. A trigger (more acute, even catastrophic) is something that may help precipitate disease onset or a change in disease activity in someone who is already susceptible.

Ferritin and vitamin B12 are useful examples of why this distinction matters.

Neither low ferritin nor low B12 has been established as direct triggers of Hashimoto’s. Iron deficiency may contribute to altered thyroid physiology and could plausibly act as a contributing driver in some situations, but whether it actually drives thyroid autoimmunity remains uncertain. B12 deficiency appears more often to be a downstream consequence or companion condition rather than a driver of Hashimoto’s itself.

So, how are these conditions connected?

Does one cause the other?

First, one clarification: ferritin is a protein that stores iron. Ferritin measured in blood is widely used as a marker of iron stores, so when we talk about “low ferritin affecting the thyroid,” we’re really talking about iron deficiency (WHO, 2020).

Here is where the scientific evidence currently stands on key questions:

Question: Does iron deficiency cause Hashimoto’s?
Not proven. Iron deficiency affects thyroid physiology and has been associated with thyroid autoantibodies in some studies, but causation has not been established. (Okuroglu et al., 2020; Garofalo et al., 2023)
Question: Can iron deficiency impair thyroid function?
Yes, particularly when deficiency is significant. Iron is involved in normal thyroid hormone production (Hess et al., 2002; Garofalo et al., 2023)
Question: Does Hashimoto’s cause low ferritin?
Not directly, as far as we know. We know that conditions that commonly coexist with autoimmune thyroid disease, particularly autoimmune gastritis, can impair iron absorption (Shah et al., 2021)
Question: Does Hashimoto’s cause B12 deficiency?
There is no convincing evidence that it does.
Question: Does B12 deficiency cause Hashimoto’s? Probably not directly. A major connection appears to be shared autoimmunity, especially autoimmune gastritis (Shah et al., 2021; Benites-Zapata et al., 2023)
Question: Can correcting iron or B12 deficiency improve symptoms?
Yes, when the deficiency is responsible for or contributing to those symptoms. That is different from treating Hashimoto’s itself.
Question: Do iron or B12 supplements treat Hashimoto’s?
Not established. There is no good evidence that supplementing someone who is already sufficient treats thyroid autoimmunity.

The key distinction is that thyroid function and thyroid autoimmunity are not the same thing.

Iron deficiency may affect how well the thyroid produces hormones. That does not automatically mean it causes the immune system to attack the thyroid.

And not every clinically relevant factor needs to be a driver or trigger of the autoimmune disease itself. Some factors matter because they affect thyroid function, worsen symptoms, or point to another underlying condition.

Iron has a direct role in thyroid function

Iron is required for the normal activity of thyroid peroxidase (TPO), one of the key enzymes involved in thyroid hormone synthesis. You might have heard of TPO from your blood test if you have Hashimoto’s disease: the immune system can produce antibodies that impair its function. It's usually measured alongside TSH, T3, T4, and TG antibodies.

Experimental research has shown that iron-deficiency, anemia, can reduce TPO activity, providing a plausible explanation for why significant iron deficiency can affect thyroid function (Hess et al., 2002).

Human evidence points in the same general direction. A 2023 systematic review and meta-analysis found significant associations between iron deficiency and alterations in thyroid hormone levels, although results varied across populations and were particularly influenced by studies in women of reproductive age and pregnancy (Garofalo et al., 2023).

So there is reasonable evidence for:

Iron deficiency → altered thyroid physiology

This makes iron deficiency biologically plausible as a contributing driver of thyroid dysfunction.

What remains much less certain is:

Iron deficiency → Hashimoto’s autoimmune disease

Multiple observational studies have reported increased levels of thyroid autoantibodies in individuals with iron deficiency. For example, a study involving 358 women of reproductive age (all with normal thyroid function) showed that 36% of iron-deficient women tested positive for thyroid antibodies, compared to 21% of control subjects (Okuroglu et al., 2020).

While interesting, it does not establish that iron deficiency caused the autoimmune response. Since the study was observational, iron deficiency might influence autoimmunity, autoimmune changes could affect iron levels, or a third factor could be involved in both.

For now, the best conclusion is: Iron deficiency may act as a potential driver of altered thyroid physiology, but whether it drives or triggers Hashimoto’s autoimmunity remains unresolved.

Does Hashimoto’s cause low ferritin?

Not necessarily. If someone with Hashimoto’s has depleted iron stores, a more relevant question is often: Why is the iron low? Causes may include heavy menstrual bleeding, pregnancy, frequent blood donation, low dietary iron intake, gastrointestinal blood loss, celiac disease, or absorption issues. A low ferritin level is not always a direct cause or trigger of Hashimoto’s; it could be an indirect sign of another underlying condition occurring alongside it. For those with Hashimoto’s, autoimmune gastritis is a specific condition that warrants attention.

The connection between Hashimoto’s, iron, and B12: autoimmune gastritis

Autoimmune thyroid disease can often coexist with other autoimmune disorders, such as autoimmune gastritis. In this condition, the immune system targets parietal cells in the stomach (Tozzoli et al., 2010; Shah et al., 2021). Parietal cells secrete stomach acid, which facilitates iron absorption. These cells also produce intrinsic factor, which is essential for vitamin B12 absorption.

As autoimmune gastritis advances, decreased stomach acid can cause iron deficiency. Over time, loss of intrinsic factor may result in vitamin B12 deficiency and, in severe cases, pernicious anemia. Typically, iron deficiency manifests before B12 deficiency in autoimmune gastritis (Shah et al., 2021). This suggests the connection might be better understood as a shared autoimmune susceptibility leading to Hashimoto’s, rather than a direct progression from Hashimoto’s to iron or B12 deficiency.

In this model, shared autoimmune susceptibility may acts more like an underlying driver, while low iron and low B12 are often downstream consequences rather than direct triggers of Hashimoto’s.

This distinction matters.

Hashimoto’s does not necessarily lead to autoimmune gastritis. Instead, having autoimmune thyroid disease may indicate the presence of another autoimmune condition. The connection is significant. In a study involving 840 individuals with Hashimoto’s, 21.4% tested positive for anti-parietal-cell antibodies, which can signal autoimmune gastritis (Boutzios et al., 2022). Another prospective study of 208 people with autoimmune thyroid disease found that 24.5% had parietal-cell antibodies; some of these individuals developed autoimmune gastritis over five years. While the presence of parietal-cell antibodies alone does not confirm autoimmune gastritis, these studies show that gastric and thyroid autoimmunity often co-occur.

What about B12?

Vitamin B12 is vital for normal nerve function, red blood cell production, and DNA synthesis. Unlike iron, there’s no strong evidence that B12 deficiency directly causes thyroid hormone failure or triggers Hashimoto’s disease. A 2023 systematic review and meta-analysis of 64 studies with over 28,000 participants found lower average B12 levels in people with hypothyroidism. However, when focusing on autoimmune thyroid disease specifically, B12 levels did not significantly differ from healthy controls. The estimated prevalence of B12 deficiency in autoimmune thyroid disease was 18%, but results varied widely among studies (Benites-Zapata et al., 2023). Therefore, B12 fits differently within the EXPIN framework compared to iron. There’s little support for the idea that low B12 is a driver or trigger of Hashimoto’s. The more plausible pathway is shared autoimmune susceptibility leading to autoimmune gastritis, which then causes B12 malabsorption. In summary, B12 deficiency is more often a downstream effect or clinical sign than a direct cause of thyroid autoimmunity.

Why can symptoms persist even when TSH is controlled?

Iron deficiency, B12 deficiency, and hypothyroidism have considerable symptom overlap.

Symptom	Hypothyroidism	Iron deficiency	B12 deficiency
Fatigue	Common	Common	Common
Weakness	Common	Common	Common
Brain fog / poor concentration	Possible	Possible	Possible
Reduced exercise tolerance	Possible	Common	Possible
Hair loss	Possible	Possible	Less typical
Feeling cold	Common	Possible	Possible
Numbness or tingling	Less typical	Less typical	Important symptom

B12 deficiency can lead to neurological issues like numbness, tingling, balance problems, and cognitive difficulties, even if anemia or enlarged red blood cells are absent (NICE, 2024). This indicates that a person can have well-regulated thyroid hormone levels and still experience symptoms that resemble hypothyroidism. However, this does not necessarily signal that Hashimoto’s is progressing or that thyroid treatment is insufficient. An alternative process might be involved. Recognizing drivers, triggers, and downstream effects is therefore valuable. A low iron or B12 level might not be the primary cause of the autoimmune condition; it could instead be:

Contributing separately to symptoms,
Influencing thyroid function,
Or indicating another underlying issue.

Once a deficiency is identified, the key question shifts from:

“Is this causing or worsening my Hashimoto’s?” to “How does this fit into the broader biological context?”

What do low ferritin or B12 levels tell me?

When low ferritin or B12 levels are detected, the numbers alone do not clarify the underlying cause. Iron deficiency can result from blood loss, greater demands, diet, or malabsorption. B12 deficiency may stem from dietary gaps, medications, gastrointestinal issues, or impaired intrinsic-factor production. In individuals with Hashimoto’s, recurrent or unexplained deficiencies in iron or B12 can hint at underlying gastrointestinal or autoimmune problems, such as autoimmune gastritis or celiac disease.

The American Gastroenterological Association recommends testing for atrophic gastritis in cases of unexplained iron or B12 deficiency, and screening patients with autoimmune gastritis for both deficiencies (Shah et al., 2021). From a cause-and-effect perspective, this matters because a low nutrient level might not be the primary problem; it could be a downstream indicator pointing to the actual trigger. Simply supplementing the nutrients may address the deficiency but does not explain why it occurred in the first place.

Is there a definitive 'optimal” ferritin level for Hashimoto’s?

This is an area where online advice often exceeds the supporting evidence. No specific ferritin target, whether 50, 70, or 100 ng/mL, has been established for Hashimoto’s. Ferritin levels are understood within a clinical context, as factors like anemia and inflammation can influence result interpretation (WHO, 2020; Ko et al., 2020). Therefore, a ferritin value should not be viewed simply as 'more is better.' The same applies to B12: correcting a deficiency is crucial, but no specific B12 level has been shown to improve Hashimoto’s autoimmunity when increased beyond a certain point.

One practical detail: iron and thyroid medication

When iron replacement is clinically indicated, timing matters for people taking levothyroxine.

Iron can reduce levothyroxine absorption (U.S. Food and Drug Administration**.** SYNTHROID (levothyroxine sodium) tablets: Prescribing Information. Revised 2024).

For people taking both medication and supplements, timing is therefore something to discuss with a clinician or pharmacist so that treating one problem does not unintentionally interfere with treatment of the other.

What does this mean in practice?

By this point, the practical implication becomes clearer.

Ferritin and B12 matter in Hashimoto’s, but not because either one has been proven to trigger the disease. They matter for three other reasons:

First, a deficiency can contribute to symptoms.

Fatigue, weakness, brain fog, hair loss, and reduced exercise tolerance can overlap substantially with hypothyroidism. A person can therefore have well-controlled thyroid hormone levels while another problem is still contributing to how they feel.

Second, iron deficiency can affect thyroid physiology itself.

Because iron is involved in thyroid hormone synthesis, significant deficiency can influence thyroid function even if it is not causing the autoimmune process.

Third, a deficiency can sometimes be a clue to something else.

If low iron or B12 is recurrent or difficult to explain, the important question may not simply be how to replace it, but why it became low. Depending on the individual situation, factors such as blood loss, diet, medications, impaired absorption, celiac disease, or autoimmune gastritis may be relevant.

This is where the driver/trigger framework becomes useful again.

A nutrient deficiency may be a contributing factor → a symptom amplifier → or a signal of another driver rather than the trigger for Hashimoto’s itself.

The broader principle is:

identify the finding → understand where it sits in the causal chain → address what is actually relevant.

That is more useful than assuming every abnormal nutrient level is either the cause of Hashimoto’s or something that simply needs to be pushed higher.

The bottom line

The relationship between Hashimoto’s, ferritin, and vitamin B12 is real — but it is not a simple cause-and-effect.

Iron deficiency can interfere with thyroid function, but it has not been proven to cause or trigger Hashimoto’s.

B12 deficiency has not been established as a driver or trigger of Hashimoto’s.

And Hashimoto’s does not directly explain every case of low iron or B12. In some people, the connection may instead reflect another autoimmune condition, such as autoimmune gastritis, that shares the same underlying susceptibility.

That distinction matters because not every relevant factor sits at the beginning of the disease process.

Some are drivers.

Some may act as triggers.

Others are downstream effects that still influence symptoms—or point to something important happening elsewhere.

Understanding which role a factor is playing is the first step toward making the science personally meaningful.

References

World Health Organization. WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations. Geneva: WHO; 2020.

Okuroglu N, Ozturk A, Özdemir A. Is iron deficiency a risk factor for the development of thyroid autoantibodies in euthyroid women with reproductive ages? Acta Endocrinologica. 2020;16(1):49–52. doi:10.4183/aeb.2020.49. PMID: 32685038.

Garofalo V, Condorelli RA, Cannarella R, Aversa A, Calogero AE, La Vignera S. Relationship between Iron Deficiency and Thyroid Function: A Systematic Review and Meta-Analysis. Nutrients. 2023;15(22):4790. doi:10.3390/nu15224790.

Hess SY, Zimmermann MB, Arnold M, Langhans W, Hurrell RF. Iron deficiency anemia reduces thyroid peroxidase activity in rats. Journal of Nutrition. 2002;132(7):1951–1955. doi:10.1093/jn/132.7.1951. PMID: 12097675.

Shah SC, Piazuelo MB, Kuipers EJ, Li D. AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review. Gastroenterology. 2021;161(4):1325–1332.e7. doi:10.1053/j.gastro.2021.06.078. PMID: 34454714.

Benites-Zapata VA, Ignacio-Cconchoy FL, Ulloque-Badaracco JR, et al. Vitamin B12 levels in thyroid disorders: a systematic review and meta-analysis. Frontiers in Endocrinology. 2023;14:1070592. doi:10.3389/fendo.2023.1070592. PMID: 36909313.

Tozzoli R, Kodermaz G, Perosa AR, et al. Autoantibodies to parietal cells as predictors of atrophic body gastritis: a five-year prospective study in patients with autoimmune thyroid diseases. Autoimmunity Reviews. 2010;10(2):80–83. doi:10.1016/j.autrev.2010.08.006. PMID: 20696284.

Boutzios G, Koukoulioti E, Goules AV, et al. Hashimoto Thyroiditis, Anti-Parietal Cell Antibodies: Associations With Autoimmune Diseases and Malignancies. Frontiers in Endocrinology. 2022;13:860880. doi:10.3389/fendo.2022.860880.

National Institute for Health and Care Excellence (NICE). Vitamin B12 deficiency in over 16s: diagnosis and management (NG239). Published March 2024.

Roy A, Laszkowska M, Sundström J, et al. Prevalence of Celiac Disease in Patients with Autoimmune Thyroid Disease: A Meta-Analysis. Thyroid. 2016;26(7):880–890. doi:10.1089/thy.2016.0108. PMID: 27256300.

U.S. Food and Drug Administration. Levothyroxine Sodium Tablets: Prescribing Information. 2023.

This article is intended for educational purposes and does not replace individualized medical evaluation, diagnosis, or treatment.