Study: Millions Treated for Hypothyroidism at Risk of Lung Cancer


7th September 2013

By  Sayer Ji

Contributing Writer for  Wake Up World

A study has uncovered a link between the synthetic thyroid hormone (trade name Synthroid) used to treat millions diagnosed with hypothyroidism and lung cancer, bringing to the forefront the harmful role that overdiagnosis and overtreatment plays in nutritional deficiency and chemical exposure related ‘diseases.’

An Italian study published in the journal Reproductive Biology and Endocrinology, titled “Levothyroxine and lung cancer in females: the importance of oxidative stress,” has raised a concerning possibility: levothyroxine (T4), one of the world’s most commonly prescribed forms of hormone replacement, may be raising the risk of lung cancer in millions of men and women being treated for low thyroid function (hypothyroidism). The authors of the study pointed out that levothyroxine (T4) treatment can lead to medication-induced (iatrogenic) thyroid over-activity (hyperthyroidism) and oxidative stress that can lead to a significant patient discomfort. They also noted that oxidative stress is one of the causes of chronic diseases and cancer.

The study looked at the prevalence of breast, colorectal, gastric and lung cancer in 18 Italian Regions during 2010 and correlated this data with sales of LT4 in 2009, focusing on women aged 30-84. (They noted that this age range corresponds to more than 80% of the consumers of the drug and to about 99% of all malignant cancers). They then correlated drug sales with cancers, eliminating the contribution of age and smoking for lung cancer risk.   They found no significant correlation between T4 sales and breast, colorectal and gastric  cancers,  but did find a significant correlation for lung cancer  (p < 0.05) corrected for smoking and age.

In discussing their findings, the authors noted that they could not exclude the possibility that the condition of hypothyroidism could favor the development of lung cancer. However, they pointed out that the opposite was actually described, and that “…hypothyroidism reduces the  aggressiveness of some cancers because of the presence of thyroid hormone receptors on  cancer cells, and spontaneous hypothyroidism may delay onset or reduce aggressiveness of  cancers.”[1]

Other research indicating that increased thyroid activity (hyperthyroidism) contributes to lung cancer pathogenesis was presented, including:

  • T4 has been reported as one of the several endogenous factors capable of supporting proliferation of lung cancer cells.[2]
  • The observation that patients with small cell carcinoma of the lung often present symptoms suggestive of hyperthyroidism (i.e. weight loss, anorexia) was made many years ago together with an over production of both T4 and T3.[3]
  • An old clinical observation on the relationship between lung cancer and thyroid function reported that patients were characterized by a low concentration of T3 and an increased T4/T3 ratio due to a decrease of 5′-monodeiodination (DI).[4]
  • DI activity in lung cancer was found to be lower than in peripheral lung tissue.[5]

The authors also cite animal experimental research which has shown that T4 increases the oxidative stress[6]  and spontaneous pulmonary metastases in mice.[7]  They also elaborate on a mechanism of T4-induced lung tissue toxicity:

[I]n rats lung the deiodination of LT4 is the lowest compared to all the other tissues.[8]  This means that the amount of LT4 reaching the lungs following an external supplementation cannot to be transformed into LT3 as in the other tissues, and make lungs very vulnerable to possible toxic effects of LT4.

The authors delved deeper into the reason why oxidative stress taking place during T4 treatment is particularly linked to lung cancer only:

The hypothesis could be that in lungs the increase of hypoxia-induced factor (HIF-1) which is determined by T4 can make oxygen much more available, increasing locally the oxidative stress together with a dangerous angiogenesis stimulation.[9]  [10]  [11]   Although we should never forget that LT4 is a life-saving thyroid hormone replacement, and that one should not exclude that the pathological reason that leads to the prescription of LT4 could favor the lung cancer development also.

The authors expanded on their findings further:

However, the impression we get from our experience in epidemiological studies monitoring[12]  is that this drug should be prescribed more cautiously. Considering that the population in Italy is about 60 million people and the sales of LT4 in the country in 2010 were 17.69 million boxes (+ 6% Vs 2009), hypothyroidism, which is the main reason for the prescription, should be a real national concern (almost 0.7 boxes/women/year). Most of the time, doctors tell patients treated with LT4 that any side effects will be temporary and almost ineluctable, and are usually dealt with through dose reduction. Assessment of oxidative stress and its balance has not been taken into consideration up to now as it should be.

Finally, they pointed out that T4, which is a synthetic form of thyroid hormone, might be avoided if T3 or the desiccated pig-derived form known as Armour Thyroid was used to control the oxidative-stress producing hydroperoxides.


Biomedicine today is awash in controversy associated with the overdiagnosis and overtreatment of asymptomatic populations. With the 2013 announcement by a National Cancer Institute commissioned expert panel that a variety of so-called ‘indolent’ neoplasms such as ductal carcinoma in situ (DCIS) and high-grade prostatic intraepithelial neoplasia (HGPIN), formerly understood to be forms of breast and prostate cancers, respectively, should be renamed to reflect their intrinsic benignity, a veritable sea change is occurring within the conventional medical establishment. Millions of people who were not only wrongly diagnosed with ‘cancers’ and subsequently aggressively treated for them with chemotherapy, radiation and surgery, are now being told that they would have been better left undiagnosed and untreated. Or, simply look at what the young-adult, T-score based definition of osteoporosis and osteopenia has done to convert millions of healthy middle-age and older women into drug-treatable patients, or, what the lipid hypothesis of cardiovascular disease causation has done to create a 30-billion dollar a year market in statin drugs, to fully appreciate the harms of overdiagnosis and overtreatment.


The increasingly global medical-industrial complex has begun to co-opt all aspects of the natural human bodily life cycle, and all the organ systems within it, as potential targets of medical surveillance and intervention, not excluding the human thyroid. According to data from the National Health and Nutrition Examination Survey, years 1988-1994,  [13]  while 0.3% of the American population exhibits overt symptoms of hypothyroidism, 14 times more   (4.3%) have so-called ‘subclinical’ hypothyroidism only detected via blood work. This relatively symptom-free reservoir of ‘hypothyroid’ cases provides a veritable gold mine of potential office visits, billable services and drug prescriptions.

The reality is that most cases of hypothyroidism today are diagnosed in populations who are experiencing a combination of basic nutritional deficiencies and chemical exposures, or who are simply going through a temporary down-cycle in thyroid function following a natural change, such as the natural postpartum drop that occurs in women after giving birth. Even acute bouts of stress and subclinical adrenal insufficiency can cause cyclical downshifts in thyroid function. At, we have indexed plenty of peer-reviewed research on over 30 natural substances, including nutrients and minerals, which may help to resolve low thyroid function, and conversely, over 30 unnatural substances, e.g. rocket fuel, pesticides, fluoride, which induce low thyroid function. View the data on GreenMedInfo’s Hypothyroidism Research  page.

Given the clear role that selenium deficiency plays in preventing the conversion of T4 to the far more biologically active form of thyroid hormone known as triiodothyronine (T3), which can cause an elevation of thyroxine-stimulating hormone (TSH), why call a mineral deficiency-induced decrease in T4 a monolithic disease entity such as “hypothyroidism”? Why not simply call it selenium deficiency? Or, if fluoride, mercury, or any number of xenobiotic chemicals in the environment requiring selenium-dependent glutathione-mediated detoxification is causing the “low thyroid,” why call chemical poisoning “hypothyroidism”? The omnipresent environmental contaminant perchlorate, an ingredient in jet fuel, is also a primary cause of hypothyroidism, but is almost never tested for by the conventional endocrinologists in their patient evaluations.

Furthermore, the geometric expansion of hypothyroidism cases in the past decade only thinly conceals an agenda to promote the synthetic form of T4 known as levothyroxine sodium (trade name Synthroid), since with each new ‘disease’ case the patient is converted into a lifelong customer. Marketed as superior to traditional glandular forms extracted from pigs (whose endocrine glands are far more bioidentical than any other animal we know of) due to the dose-to-dose standardization of the so-called   ‘active ingredient’ T4 versus the natural variations in hormone concentrations found in the ‘real thing,’ which incidentally contains a wide range of additional hormones including T1, T2, T3, all of which are vitally important.

One of the main drawbacks of administering T4 in isolation is the possibility that it will not convert adequately to T3, and will therefore ‘back up’ causing excessive T4 activity, i.e. hyperthyroidism. There is also the very real possibility that T4 will not only not properly interact with thyroxine cellular receptors, but will block out what remaining natural levothyroxine the thyroid is still producing (and whose conformational state is far more health-promoting), essentially acting as an endocrine disrupter at the very moment that it is acting as intended as a ‘TSH suppressor.’ This T4 blocking/endocrine-disrupting property of the synthetic form would also activate a negative feedback loop within the endocrine system, further suppressing remaining thyroid function, and resulting in the atrophy of the compromised thyroid, a iatrogenic ‘self-fulfilling prophecy’ if you will.

Overtreatment, of course, is the hallmark danger of overdiagnosis. Whereas a patient who had suboptimal thyroid function, but did not have noticeable symptoms, is suddenly given pharmacological doses of synthetic T4 and suddenly experiences the wide range of acute, adverse health effects associated with a now hyperactive and/or increasingly disrupted thyroid, as a result.

Indeed, research indicates that hypothyroid patients treated with T4 replacement, that is sufficient to maintain a normal serum TSH, actually have serum free T4 that is higher than in untreated normal patients and may not result in appropriately normal serum free T3 concentrations.[14]   In other words, you can ‘normalize’ the main clinically measurable parameter associated with ‘low thyroid function,’ i.e. elevated TSH, without actually improving the overall physiological situation, nor the patient’s subjective experience of well being.

There is also compelling research indicating that desiccated thyroid extract (Armour thyroid) results in superior clinical outcomes versus the synthetic hormone, especially as concerns improved body weight.[15]  [16]There is also the more logical option of support the body’s thyroid-hormone producing capabilities using the thyroxine precursor  L-tyrosine, a basic amino acid with a relatively high margin of safety. In fact,  a 2004 study  in subjects with normal thyroid function found that administration of tyrosine leads to a significant reduction in serum TSH and improvement in mood in winter compared with placebo, while the combined synthetic T4-T3 supplement leads to a worsening of mood in summer and no improvement in winter, indicating supporting glandular function is superior to ‘replacement’ therapy, as well as the role seasonality may play in hormone function and hormone treatment interventions.

Ultimately, this Italian study brings further attention to one of a wide range of unintended, adverse health effects associated with the overdiagnosis and subsequent overtreatment of hypothyroidism, and the underlying failure of the conventional, largely drug-based paradigm to comprehend the causes and real solutions of disease and human suffering.

Article references:

  • [1]  Hercbergs AH, Ashur-Fabian O, Garfield D: Thyroid hormone and cancer: clinical studies of hypothyroidism in oncology. Curr Opin Endocrinol Diabetes Obes 2010, 17:432–436.
  • [2]  Meng R, Tang HY, Westfall J, London D, Cao JH, Mousa SA, Luidens M, Hercbergs A, Davis FB, Davis PJ, et al: Crosstalk between integrin αvβ3 and estrogen receptor-α is involved in thyroid hormone-induced proliferation in human lung carcinoma cells. PLoSone 2011, 11:e27547.
  • [3]Faber J, Poulsen S, Iversen P, Kirkegaard C: Thyroid hormone turnover in patients with small cell carcinoma of the lung. Acta Endocrinol 1988, 118:460–464.
  • [4]  Ratcliffe JG, Stack BH, Burt RW, Radcliffe WA, Spilg WG, Cuthbert J, Kennedy RS: Thyroid function in lung cancer. Brit Med J 1978, 1:210–212.
  • [5]Wawrzynska L, Sakowicz A, Rudzinski P, Langfort R, Kurzyna M: The conversion to triiodothyronine in the lung: comparison of activity of type I iodotironine 5′ deiodinase in lung cancer with peripheral lung tissues. Monaldi Arch Chest Dis 2003, 59:140–145.
  • [6]  Venditti P, Di Stefano L, Di Meo S: Oxidative stress in cold induced hyperthyroid state. J Exp Biol 2010, 213:2899–2911.
  • [7] Kinoshita S, Sone S, Yamashita T, Tsubura E, Ogura T: Effects of experimental hyperand hypothyroidism on natural defense activities against Lewis lung carcinoma and its spontaneous pulmonary metastases in C57BL/6 mice. Tokushima J Exp Med 1991, 38:25–35.
  • [8]  van Doorn J, Roelfsema F, van der Heide D: Concentration of thyroxine and 3,5,3′-triiodotyronine in several rat tissue in vivo: the effect of hypothyroidism. Endocrinology 1985, 117:1201–1208.
  • [9]  Otto T, Fandrey J: Thyroid hormone induces hypoxia-inducible factor 1α gene expression through thyroid hormone receptor β/retinoid x receptor α-dependent activation of hepatic leukemia factor. Endocrinology 2008, 149:2241–2250.
  • [10]  Hofer T, Desbaillets I, Höpfl G, Wenger RH, Gassmann M: Characterization of HIFD-1 alpha overexpressing Hela cells and implication for gene therapy. Comp Biochem Physiol C Toxicol Pharmacol 2002, 133:475–481.
  • [11]  Wan J, Chai H, Yu Z, Ge W, Kang N, Xia W, Che Y: H1F-1α on angiogenic potential in human small cell carcinoma. Clin Cancer Res 2011, 30:77.
  • [12]  Cesarone MR, Belcaro G, Nicolaides AN, Incandela L, De Sanctis MT, Barsotti A: San Valentino epidemiologic project. Angiology 2000, 51:S65–S68.
  • [13]  Hollowell JG, Staehling NW, Flanders WD,  et al.  (February 2002).  “Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III)”.  J. Clin. Endocrinol. Metab.87  (2): 489–99.  PMID  11836274.
  • [14] K A Woeber.  Levothyroxine therapy and serum free thyroxine and free triiodothyronine concentrations.  J Endocrinol Invest. 2002 Feb ;25(2):106-9. PMID:  11929079
  • [15]  Thanh D Hoang, Cara H Olsen, Vinh Q Mai, Patrick W Clyde, Mohamed K M Shakir.  Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: a randomized, double-blind, crossover study.  J Clin Endocrinol Metab. 2013 May ;98(5):1982-90. Epub 2013 Mar 28. PMID:  23539727
  • [16]  Alan R Gaby.  Sub-laboratory hypothyroidism and the empirical use of Armour thyroid.  Altern Med Rev. 2004 Jun;9(2):157-79. PMID:  15253676

About the author:


Sayer Ji is the founder of, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, and Steering Committee Member of the Global Non-GMO Foundation.

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