Nicotine and Hashimoto’s Thyroiditis: Dr. Ardis on Hypothyroidism

Hashimoto’s thyroiditis is the most common cause of an underactive thyroid in countries with enough iodine in the diet: the immune system slowly attacks the thyroid gland until it can no longer make enough hormone. Dr. Bryan Ardis states that nicotine can cure the symptoms of hypothyroidism in women and in men, and that a person with Hashimoto’s “should be on nicotine just like my wife.” He wears a nicotine patch himself every day and says he will for the rest of his life.

This page sets out what Dr. Ardis says, then walks through the research on the subject: the large population surveys in the United States, Denmark and Norway that measured thyroid antibodies and thyroid function in smokers and non-smokers; the studies that followed people after they stopped smoking; a Japanese study of smokers who already had Hashimoto’s; what is known about how tobacco smoke and nicotine act on the thyroid; the separate story of Graves’ disease and Graves’ eye disease; and the small amount of work done on tobacco alkaloids themselves.

Table of Contents

  1. 1. What Dr. Ardis Says
  2. 2. A Plain Primer: Hashimoto’s and Hypothyroidism
  3. 3. Smokers and Thyroid Antibodies: NHANES III and Denmark
  4. 4. Smoking and Thyroid Function: The Norwegian HUNT Study
  5. 5. What the Studies Recorded After People Quit
  6. 6. Smoking in People Who Already Have Hashimoto’s
  7. 7. Nicotine, Thiocyanate and the Thyroid
  8. 8. Graves’ Disease and Graves’ Eye Disease
  9. 9. Nicotine and Tobacco Alkaloids on Their Own
  10. Safety Notes
  11. Dr. Ardis’s Own Work
  12. Key Research Papers
  13. Connections
  14. Featured Videos

1. What Dr. Ardis Says

Dr. Ardis set this out in a 2025 podcast appearance (Culture Apothecary) and in his book Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity. He raises the thyroid in a run of conditions he says nicotine has been published to help, straight after ulcerative colitis, which he describes as an autoimmune digestive disorder that nicotine is published to cure.

His statements on the thyroid, in his order:

Dr. Ardis frames these points as part of a body of published science that, in his words, doctors “weren’t taught in med school.” He does not name a specific thyroid study in this passage. The specific study is not identified here; related published work is listed below.

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2. A Plain Primer: Hashimoto’s and Hypothyroidism

The thyroid is a butterfly-shaped gland at the front of the neck. It takes iodine from the blood and uses it to make two hormones, T4 and T3, which set the pace of almost every cell in the body. When it makes too little, the result is hypothyroidism: tiredness, feeling cold, weight gain, dry skin, constipation, slowed thinking, low mood and heavy periods are common complaints.

The brain watches the thyroid through a hormone called TSH (thyroid-stimulating hormone). When thyroid hormone runs low, the pituitary gland pushes TSH up to drive the thyroid harder. A high TSH is therefore the usual blood-test sign of an underactive thyroid, and a low TSH the sign of an overactive one.

In Hashimoto’s thyroiditis the immune system turns against the gland. Two antibodies are the markers doctors test for:

Many people carry these antibodies for years with a normal TSH; some go on to develop hypothyroidism. That gap — between having antibodies and losing thyroid function — is why the studies below measure both. Hashimoto’s is far more common in women than in men.

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3. Smokers and Thyroid Antibodies: NHANES III and Denmark

The United States: NHANES III (Belin, 2004)

The Third National Health and Nutrition Examination Survey (NHANES III), run from 1988 to 1994, sampled people to represent the whole non-institutionalised population of the United States. A Johns Hopkins team led by Robert Belin analysed thyroid tests from 15,592 people who were not taking thyroid-altering medicines. Rather than relying on what people said about their smoking, they classed anyone with a blood cotinine (a breakdown product of nicotine) above 15 ng/mL as a smoker.

The authors wrote that smoking “appears to be negatively associated with serological evidence of thyroid autoimmunity and hypothyroidism and positively associated with mild TSH decreases,” and that understanding the mechanism could point to ways of preventing autoimmune thyroid disease. Because it is a single snapshot in time, the survey shows an association rather than a cause.

Denmark: the DanThyr population study (Pedersen, 2008)

In two areas of Denmark with moderate and mild iodine deficiency, Inge Bülow Pedersen and colleagues examined 4,649 randomly selected adults aged 18 to 65. Smoking was associated with a lower presence of thyroid antibodies, and the link was stronger for Tg antibodies than for TPO antibodies; once Tg antibodies were taken into account, the link with TPO antibodies alone was no longer seen. The authors noted that the cross-sectional design “precludes any conclusions as to the cause” of the association.

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4. Smoking and Thyroid Function: The Norwegian HUNT Study

Between 1995 and 1997, the HUNT health survey in Nord-Trøndelag, Norway, measured TSH in 20,479 women and 10,355 men with no previously known thyroid disease. Bjørn Åsvold and colleagues compared current, former and never smokers.

The authors concluded that smoking is negatively associated with hypothyroidism and positively associated with hyperthyroidism, and that the pattern after quitting suggests the effects are reversible. They reported this as the first description of a lower prevalence of overt hypothyroidism among current smokers.

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5. What the Studies Recorded After People Quit

Amsterdam: women followed for five years (Effraimidis, 2009)

Grigoris Effraimidis, Jan Tijssen and Wilmar Wiersinga followed 521 women in the Netherlands for five years. All had a relative with autoimmune thyroid disease, all had normal thyroid function, and none had thyroid antibodies at the start. Over five years, 20.1% developed TPO and/or Tg antibodies. When each woman who developed antibodies was compared with two matched women who did not, the groups were alike in every exposure measured except smoking: current smoking fell among the women who went on to develop antibodies. The odds ratio for current smoking at the time antibodies appeared was 0.59. The authors concluded that stopping smoking “is associated with an increased risk for occurrence of TPO-Ab and/or Tg-Ab in serum,” in line with the lower risk of hypothyroidism in smokers. The study appeared in the Journal of Clinical Endocrinology & Metabolism.

Denmark: new cases of autoimmune hypothyroidism (Carlé, 2012)

Allan Carlé and colleagues monitored every thyroid function test performed in two defined regions of Denmark — just over two million person-years of observation — and identified 140 people newly diagnosed with overt autoimmune hypothyroidism. Each was matched with four people of the same age, sex and region with normal thyroid function (560 controls). Smoking habits were confirmed by measuring urinary cotinine.

The authors described the rise as “sharp but transient.” They wrote that smoking cessation “is vital to prevent death and severe disease,” and that awareness of hypothyroidism should be high in people who have recently quit, with “virtually any complaint” prompting a thyroid test.

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6. Smoking in People Who Already Have Hashimoto’s

The studies above look at whole populations, most of whom never develop thyroid disease. One retrospective study looked instead at people already diagnosed. At Kuma Hospital in Kobe, Japan, Shuji Fukata and colleagues reviewed 387 women with Hashimoto’s thyroiditis.

The authors suggested that thiocyanate from smoking may contribute to hypothyroidism in people who already have Hashimoto’s. Read beside the population studies, this means the published work on smoking points in two directions depending on the group studied: fewer antibodies and less hypothyroidism in general populations, and more hypothyroidism among the Hashimoto’s patients in this Japanese series. These were cigarette smokers; thiocyanate comes from the smoke, not from nicotine.

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7. Nicotine, Thiocyanate and the Thyroid

Tobacco smoke carries thousands of compounds, so a finding in smokers does not by itself say which compound is responsible. Researchers have pointed to two main routes.

Nicotine and the nervous system

In a 2013 review in Clinical Endocrinology, Wilmar Wiersinga described the slight, dose-dependent fall in TSH seen in smokers as likely secondary to a rise in free T4 and free T3 brought on by activation of the sympathetic (“fight or flight”) nervous system — an effect independent of iodine intake. Nicotine is a well-known activator of that system. The same review states that current smoking lowers the risk of developing TPO and Tg antibodies and of subclinical and overt autoimmune hypothyroidism, that the effect is dose dependent and disappears within three years of quitting, and that evidence from an animal model of experimental autoimmune thyroiditis points to anti-inflammatory effects of nicotine. Dr. Ardis’s wider argument that nicotine acts on the body’s anti-inflammatory nicotinic receptors is set out on the nicotinic acetylcholine receptors page.

Thiocyanate and iodine

Burning tobacco releases cyanide, which the body converts to thiocyanate. Thiocyanate competes with iodide for the pump the thyroid uses to take iodine in. A 2017 review by Marie-Emilie Willemin and Annie Lumen at the FDA’s National Center for Toxicological Research notes that people are exposed to thiocyanate mainly through diet (cruciferous vegetables such as cabbage contain its precursors) and cigarette smoke, and that it also interferes with the enzyme steps that attach iodine to thyroid hormone. Wiersinga’s review links the slightly larger thyroids of smokers to this iodine competition, seen in iodine-deficient areas but not in iodine-sufficient ones. A nicotine patch delivers nicotine without combustion, so it does not produce this smoke-derived thiocyanate.

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8. Graves’ Disease and Graves’ Eye Disease

Graves’ disease is the other common autoimmune thyroid disease: instead of destroying the gland, antibodies stimulate it, causing an overactive thyroid. In some people the immune attack also reaches the tissue behind the eyes, causing Graves’ ophthalmopathy (also called Graves’ orbitopathy or thyroid eye disease) — bulging, gritty, swollen eyes and sometimes double vision.

These findings concern smoking, not nicotine on its own; the studies do not separate the two. Readers with Graves’ disease or a history of thyroid eye disease are a distinct group from readers with Hashimoto’s.

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9. Nicotine and Tobacco Alkaloids on Their Own

Every human study above measured smoking — by questionnaire or by cotinine, the nicotine breakdown product that marks tobacco or nicotine exposure. Studies that give nicotine alone to people with thyroid disease are far fewer.

For scale: the nicotine patches sold for quitting smoking come mainly in 7, 14 and 21 mg strengths, each delivering that amount over about 24 hours. The 3.5 mg daily amount Dr. Ardis describes for himself is half of the smallest common strength. The site’s Nicotine Patch Protocol page sets out the adult strengths and the half-patch approach.

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Safety Notes

The full list of contraindications, drug interactions and side effects is on the Nicotine Patch Protocol page.

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Dr. Ardis’s Own Work

  1. Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity — his book, where the nicotine thread runs through the recovery chapters.
  2. The Dr. Bryan Ardis hub — his nicotine hypothesis and snake-venom theory, with every page in this wing.
  3. Culture Apothecary podcast, “Nicotine Is NOT the Villain” (2025) — the source of the statements in section 1.
  4. The Dr. Ardis Show — official site

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Key Research Papers

  1. Belin RM, Astor BC, Powe NR, Ladenson PW (2004). Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin concentration elevation and a higher prevalence of mild thyrotropin concentration suppression in the third National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab. — PubMed PMID: 15579761
  2. Pedersen IB, Laurberg P, Knudsen N, et al. (2008). Smoking is negatively associated with the presence of thyroglobulin autoantibody and to a lesser degree with thyroid peroxidase autoantibody in serum: a population study. Eur J Endocrinol. — PubMed PMID: 18299471
  3. Asvold BO, Bjøro T, Nilsen TI, Vatten LJ (2007). Tobacco smoking and thyroid function: a population-based study. Arch Intern Med. — PubMed PMID: 17620538
  4. Effraimidis G, Tijssen JG, Wiersinga WM (2009). Discontinuation of smoking increases the risk for developing thyroid peroxidase antibodies and/or thyroglobulin antibodies: a prospective study. J Clin Endocrinol Metab. — PubMed PMID: 19141579
  5. Carlé A, Bülow Pedersen I, Knudsen N, et al. (2012). Smoking cessation is followed by a sharp but transient rise in the incidence of overt autoimmune hypothyroidism – a population-based, case-control study. Clin Endocrinol (Oxf). — PubMed PMID: 22651374
  6. Fukata S, Kuma K, Sugawara M (1996). Relationship between cigarette smoking and hypothyroidism in patients with Hashimoto’s thyroiditis. J Endocrinol Invest. — PubMed PMID: 8957745
  7. Wiersinga WM (2013). Smoking and thyroid. Clin Endocrinol (Oxf). — PubMed PMID: 23581474
  8. Willemin ME, Lumen A (2017). Thiocyanate: a review and evaluation of the kinetics and the modes of action for thyroid hormone perturbations. Crit Rev Toxicol. — PubMed PMID: 28632039
  9. Prummel MF, Wiersinga WM (1993). Smoking and risk of Graves’ disease. JAMA. — PubMed PMID: 8419666
  10. Vestergaard P (2002). Smoking and thyroid disorders – a meta-analysis. Eur J Endocrinol. — PubMed PMID: 11834423
  11. Bartalena L, Kahaly GJ, Baldeschi L, et al. (2021). The 2021 European Group on Graves’ orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves’ orbitopathy. Eur J Endocrinol. — PubMed PMID: 34297684
  12. Caturegli P, De Remigis A, Ferlito M, et al. (2012). Anatabine ameliorates experimental autoimmune thyroiditis. Endocrinology. — PubMed PMID: 22807490

PubMed Topic Searches

  1. PubMed: Smoking and thyroid autoantibodies
  2. PubMed: Smoking cessation and autoimmune hypothyroidism
  3. PubMed: Nicotine and autoimmune thyroiditis

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Connections

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