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Weight Gain, Hypothyroidism and Smoking Cessation

Published online by Cambridge University Press:  13 May 2016

Renee Bittoun,
Ash Gargya and
Linda Mann
Renee Bittoun*
Affiliation:
Royal Prince Alfred Hospital, Sydney Local Health District and The Smoking Research Unit, University of Sydney, Sydney, NSW, Australia
Ash Gargya
Affiliation:
Department of Endocrinology, Royal Prince Alfred Hospital, Sydney Local Health District, Sydney, NSW, Australia
Linda Mann
Affiliation:
Your Doctors, General Medical Practice, Sydney, NSW, Australia
*
Address for correspondence: Renee Bittoun, Smoking Research Unit, Brain Mind Research Centre, University of Sydney, Sydney, NSW, Australia. Email: renee.bittoun@sydney.edu.au
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Extract

The case study received ethics approval from Sydney Local Health District Ethics Review Committee.

Information

Type
Protocol
Information
Journal of Smoking Cessation , Volume 12 , Issue 2 , June 2017, pp. 86 - 87
Copyright
Copyright © The Author(s) 2016 

The case study received ethics approval from Sydney Local Health District Ethics Review Committee.

A Case Report

A 71-year old Caucasian woman presented for smoking cessation advice and management. She had a long history of smoking for more than 50 years with multiple unsuccessful attempts at quitting. She had risk factors for potential smoking related diseases but was well on presentation. She smoked between 10 to 17 cigarettes/day (c/d) and her time to first cigarette (TTFC) was within 5 minutes of waking (a significant sign of dependence). Her base-line expired Carbon Monoxide (CO) reading was 23 parts per million (ppm). Normal Australian non-smoking values are 2.75 ppm (±0.75 ppm) (Bittoun, Kentaro, Elcombe, & Takata, Reference Bittoun, Kentaro, Elcombe and Takata2014). She was commenced on nicotine replacement therapy (NRT) of one 21mg nicotine 24 hour patch. On weekly follow-ups, she reduced her smoking to 5 c/d as more NRT in the form of a second patch was added. Her expired CO dropped concomitantly to 6 ppm and when oral nicotine strips were added to the regimen, she ceased smoking altogether. This was confirmed with regular expired CO readings of 2 ppm (Bittoun et al., Reference Bittoun, Kentaro, Elcombe and Takata2014). After two weeks, the additional 21mg patch was ceased and she remained on one nicotine patch for more than two months, her self-reported abstinence from smoking continuously confirmed by expired CO tests. During this time, however, she became concerned about her rapid weight gain of more than 10 kg and symptoms of low mood and increasing anxiety. As these are common symptoms of nicotine withdrawal, NRT was adjusted and increased accordingly.

After several months of smoking abstinence, she reported to her doctor (LM) for her routine blood tests and it was found that her Thyroid Stimulating Hormone (TSH) had abruptly risen from 4.67 mIU/L prior to smoking cessationFootnote 1 to 51.2 mIU/L (normal value 0.4 to 5 mIU/L) post smoking cessation. She had gained 15 kg in this time and volunteered that she had both a mother and two sisters with hypothyroidism. She was immediately referred to an endocrinologist (AG) who confirmed autoimmune (Hashimoto's) hypothyroidism and commenced treatment with Thyroxine sodium. She remains smoke free and on NRT in the form of one 21mg nicotine patch per day.

Discussion

Smoking tobacco is negatively correlated with autoimmune hypothyroidism (Åsvold, Bjøro, Nilsen, & Vatten, Reference Åsvold, Bjøro, Nilsen and Vatten2007; Vestergaard, Reference Vestergaard2002; Wiersinga, Reference Wiersinga2012). It may be assumed nicotine is not the culpable agent in this case as she was on substantial doses of NRT and had no urges to smoke. Rodent studies showed that infusing nicotine had no effect on TSH, T4 or T3 (Alzoubi & Alkadhi, Reference Alzoubi and Alkadhi2014). Iodine uptake/organification may be affected by thiocyanates, not nicotine.

There may be a protective effect of anatabine, an alkaloid found in tobacco; this compound reduces thyroglobulin antibody levels in human subjects with Hashimoto's thyroiditis and seems to be positively correlated with recent quitting (Schmeltz et al., Reference Schmeltz, Blevins, Aronoff, Ozer, Leffert and Goldberg2014) even in people with no family history of the disease or any personal previous history (Krassas & Wiersinga, Reference Krassas and Wiersinga2006; Laurberg, Andersen, Pedersen, Knudsen, & Carlé, Reference Laurberg, Andersen, Pedersen, Knudsen and Carlé2013).

Based on article by Carlé et al. (Reference Carlé, Bülow Pedersen, Knudsen, Perrild, Ovesen and Banke Rasmussen2012), it appears that most cases of hypothyroidism occur in the first 2 years, mainly in the first 12 months (Carlé et al., Reference Carlé, Bülow Pedersen, Knudsen, Perrild, Ovesen and Banke Rasmussen2012). Unfortunately, some common symptoms of nicotine withdrawal (American Psychiatric Association, 2013) mimic those of hypothyroidism: weight gain, lack of concentration, depression, constipation and anxiety and thus acute hypothyroidism has been commonly overlooked as a cause of these symptoms during smoking cessation attempts and the development of these symptoms are well described risk factors for relapsing to smoking (American Psychiatric Association, 2013).

There is currently poor understanding of the mechanism of the influences smoking cessation has on thyroid autoimmunity and function and further research is required to investigate the effects that nicotine per say may have (or not) have on thyroid function.

Tobacco treatment or cessation counsellors should be alerted to this phenomenon and monitor pre and post cessation TSH in patients quitting smoking. This is particularly important in those who have had episodes of weight gain in their previous quit attempts and those with any family history of thyroid illnesses.

Financial Support

None.

Conflicts of Interest

This research received no specific grant from any funding agency, commercial or non-for-profit sectors.

Footnotes

1 Thyroid hormone levels (T3 and T4) were also assessed prior to smoking cessation. Results showed Free T4 = 6.0 pmol/L (rr 10–20 pmol/L) and Free T3 = 2.2 pmol/L (rr 2.3–5.7pmol/L) [Architect (Abbott Diagnostics, Australia)].

References

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